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1
Charoenchon, Nisamanee. "Can green tea catechin supplement protect against photoageing?" Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/can-green-tea-catechin-supplement-protect-against-photoageing(64eefb5f-ef37-4900-9c03-3477c8a74e50).html.
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Photoaged skin caused by chronic ultraviolet radiation (UVR) is characterised clinically with hyperpigmentation, coarse skin texture and deep wrinkles; the worst outcome is skin cancer. Histological investigation of the alteration within major extracellular matrices (ECM; elastic fibres, fibrillar collagens) is essential study to understand the cellular effect on skin structure from UVR. This thesis used an acute dose of radiation to examine in humans in vivo the effect of UVR on ECM components before assessing whether a dietary intervention could protect skin from UVR damage. Green tea catechins (GTCs) have anti-oxidant properties and may be an interesting option as a systemic photoprotection agent. Hence this thesis assesses: 1) the effect of acute irradiation of skin on dermal ECM damage to see whether it mimics the changes observed in photoageing and; 2) whether dietary supplementation with GTC will provide dermal ECM protection. UV-induced change in elastic fibre network. Initially, the effect of two different UV light sources on elastic fibre protein (elastic fibres, fibrillin-rich microfibrils and fibulin-2 and -5 microfibrils) remodelling was performed. The effect of ultraviolet B vs full-spectrum solar simulated radiation (SSR) were investigated in a small sample of healthy Caucasian volunteers (n = 6 per group). At 24 hour after 3× MED irradiation, Weigert's resorcin–fuchsin stained elastic fibres showed a significant reduction regardless of irradiation protocol (UVB, P<0.01; SSR P<0.05). Specific components were identified by immunohistochemistry; a significant reduction in fibrillin-rich microfibrils (FRM) was observed in UVB-irradiated skin (P<0.05), whilst fibulin-5-positive microfibrils were only affected by SSR (P<0.05). The data revealed, therefore, differential effects on UV wavelength on ECM remodelling. SSR, the more physiologically relevant light source was used in subsequent studies Supplement effect in SSR-induced damage in elastic fibre. Fifty healthy volunteers were recruited to this randomised control trial to investigate whether GTC can protect skin from photodamage. Volunteers were randomized to GTC (1080 mg plus 100 mg vitamin C; n=25) or placebo (maltodextrin; n = 25) daily for 12-weeks with compliance assessed biochemically in urine samples. Of the n = 50 recruited, 44 volunteers completed the study. In baseline, UVR challenge resulted in a significant remodeling of the cutaneous elastic fiber system (P<0.001), particularly fibulin-2 and fibulin-5-positive microfibrils at 24-hr after 3×MED irradiation. In post-supplementation, fibulin-5 positive microfibrils were protected from UVR remodeling (% staining, mean ± SE; no UV, 18.1±0.89; UVR, 17.1±0.61; P=0.30) whilst no protection was seen in the placebo group (no UVR, 19.41±0.79; UVR, 17.69±0.61; P<0.05). Supplement effect in SSR-induced damage in collagenous matrix. In the identical experiment, collagenous matrices including synthesis of procollagen I was also examined as fibrillar collagens are the major ECM components providing strength within dermis. The fibrillar collagen and newly synthesised procollagen I were stained by Picrosirius red and immunohistochemistry respectively. At baseline, acute irradiation significantly reduced papillary dermal fibrillar collagens (P<0.001) and induced deposition of newly synthesised pro-collagen I (P=0.02). In post-supplementation, GTC enhanced the deposition of thin collagen fibres in the dermis. Whilst placebo showed no effect on the altered organisation of fibrillar collagens or deposition of pro-collagen I following the irradiation challenge, GTC protected the organisation of fibrillar collagens in the papillary dermis (P=0.97).This novel in vivo human study may be used to recapitulate elastic fibre and collagen changes associated with photoageing and may be useful for dissecting out the mechanisms underlying extracellular matrix damage in response to chronic sunlight exposure. Furthermore, in a randomized control trial, dietary GTC protected fibulin-5 microfibrils and collagen fibres in the papillary dermis from UV-mediated degradation. The mechanism by which this protection occurs requires further study.
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Ahn, Jinsoo. "Characterization of (+)-Catechin and Quercetin from Pawpaw Pulp." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1307045912.
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Peng, Zhongkui. "Feeding determinants in aphids with special reference to the Rose Aphid Macrosiphum rosae (L.)." Title page, table of contents and introduction only, 1991. http://web4.library.adelaide.edu.au/theses/09PH/09php398.pdf.
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Bibliography: leaves 170-189. This thesis looks at aphid feeding determinants by type and location. It examines the role of leaf surface chemicals in the discrimination of host plants and the deterrent effect of catechin and its oxidative condensation products.
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Forrest, Neil David. "Studies on new approaches for the radiolabelling of (+)-catechin." Thesis, University of Glasgow, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410656.
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Ryle, Peter Robert. "Ethanol-induced fatty liver : protective action of (+)-catechin compounds." Thesis, University of Surrey, 1986. http://epubs.surrey.ac.uk/847975/.
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The aim of the work presented in this thesis was to assess the protective properties of the bioflavanoid drug, (+)-catechin, and its palmityl ester, 3-palmitoyl-(+)-catechin, against ethanol hepato-toxicity (ie: fatty liver) in the rat. In initial experiments, both (+)-catechin compounds were found to protect against the hepatic lipid accumulation (mainly triglyceride) after acute ethanol dosing, and after long-term feeding of ethanol in a liquid diet. In the latter situation, 3-palmitoyl-(+)-catechin was significantly more effective than (+)-catechin itself at preventing fatty liver, probably as a result of its greater lipid solubility and longer half-life in the liver tissue. Published work suggested two possible mechanisms of action for the (+)-catechin compounds against ethanol hepatotoxicity. Firstly, the ability of the drugs to correct the elevated hepatic NADH:NAD ratio (redox-state) after ethanol dosing may limit steatosis. Secondly, free radical scavenging properties may prevent liver injury occurring as a result of ethanol-induced lipid peroxidation. Acute experiments were performed which confirmed that the (+)-catechin compounds corrected the redox-state change after acute ethanol administration, but subsequent studies in which correction of the redox-state by Naloxone or Methylene Blue was found to have little influence on ethanol-induced steatosis, suggested that this was not the mechanism of action of the drugs. Synthetic antioxidants (free radical scavengers) were found to prevent both acute and chronic ethanol-induced fatty liver, under the same experimental conditions as those under which the (+)-catechin compounds afforded protection, without reversing the redox-state change after ethanol dosing. 3-Palmitoyl-(+)-catechin was then shown to prevent ethanol-induced hepatic lipid peroxidation (measured as mitochondrial diene conjugates and liver malonaldehyde levels) after acute ethanol dosing, at the same time as preventing triglyceride accumulation. As other effects of the compounds which might influence fat accumulation after ethanol were excluded (eg: inhibition of ethanol metabolism or lowering of liver acetaldehyde concentrations), it was concluded that the (+)-catechin compounds protect against alcoholic fatty liver in rats by inhibiting ethanol-induced lipid peroxidation, and the possible consequence of the latter (ie: mitochondrial damage and impaired fatty acid oxidation), rather than acting through modulation of the redox-state. The findings here cast doubts on the commonly-quoted 'redox-state' mechanism for fatty liver production by ethanol, and support the lipid peroxidation hypothesis for alcoholic liver injury.
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Lee, Suk-ching. "Effect of green tea derived compounds on the growth of androgen independent prostate cancer in vivo /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36404640.
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Kopaniszen, Malgorzata. "Protective effect of green tea polyphenols on dinitrobenzene sulphonic acid (DNBS)-induced colitis in mice." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687466.
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Chen, Jie Jack. "Growth inhibition effects of green tea and epigallocatechin gallate in bladder tumors." Click to view the E-thesis via HKUTO, 2003. http://sunzi.lib.hku.hk/hkuto/record/B4257772X.
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Yu, Sze-tak. "Effects of Chinese green tea and tea catechins on lipolysis." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21106137.
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Hsiao, Hui-Chun. "ANTHOCYANIN COLOR ENHANCEMENT BY USING CATECHIN AS COPIGMENTS AND STABILITY DURING STORAGE." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397748937.
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Majoni, Sandra. "Effects of shelf-life on phytonutrient composition in stored non-alcoholic beer." Menomonie, WI : University of Wisconsin--Stout, 2006. http://www.uwstout.edu/lib/thesis/2006/2006majonis.pdf.
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Lee, Suk-ching, and 李淑貞. "Effect of green tea derived compounds on the growth of androgen independent prostate cancer in vivo." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010808.
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Assis, Jorgiana Silva de. "Analysis of antimicrobial flavonoid epigallocatechin-3-gallate as a cavity cleansing agent in artificially carious dentin." Universidade Federal do CearÃ, 2013. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=11169.
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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgicoThe aim of this study was to evaluate the efficacy of the flavonoid epigallocatechin-3-gallate (EGCG) in concentrations of 0.5%, 1% and 2% as an antimicrobial solution in artificially carious dentin, with 2% chlorhexidine and 0.9% saline solution as controls. Twenty-five slabs of human dentin (4 mm x 4 mm) were immersed for five days in Brain Heart Infusion broth (BHI-broth) inoculated at first day with Streptococcus mutans UA159 (Batch Culture Model). On the fifth day of the experiment, the blocks were randomly divided into five groups: group I - negative control - 0.9% saline solution, group II - positive control - 2% chlorhexidine, group III - 0.5% EGCG, group IV - 1% EGCG, group V - 2% EGCG. Each slab was subjected to 15 Âl of the tested solution for 60 seconds. After treatments, artificially carious dentin was removed from the dentin slabs and analyzed by counting colony forming units (CFUs). All experiments were performed in triplicate and the data obtained in CFUs mean values converted to log base-10. The statistical tests used were analysis of variance (ANOVA) followed by Tukey test. There was no statistical difference between EGCG concentrations and saline (p > 0.05). Furthermore, there is no statistical difference between EGCG concentrations (p > 0.05). However, there was statistically significant difference between chlorhexidine and the other groups (p < 0.05). From the data obtained in this study, is possible to conclude that the substance tested is not effective on elimination of pathogen S. mutans when used in a concentration of 0.5%, 1% and 2% in artificially carious dentin.
O objetivo do presente estudo foi avaliar a eficÃcia do flavonÃide epigalocatequina-3-galato (EGCG) nas concentraÃÃes de 0,5%, 1% e 2% como soluÃÃo antimicrobiana em dentina artificialmente cariada, tendo a clorexidina 2% e a soluÃÃo salina 0,9% como controles. Vinte e cinco blocos de dentina humana (4 mm x 4 mm) foram imersos por cinco dias em BHI-caldo inoculado com Streptococcus mutans UA159 no primeiro dia do experimento. No quinto dia do experimento, os blocos foram aleatoriamente distribuÃdos em cinco grupos: grupo I â controle negativo â soluÃÃo salina 0,9%; grupo II â controle positivo â clorexidina 2%; grupo III â EGCG 0,5%; grupo IV â EGCG 1%; grupo V - EGCG 2%. Cada bloco recebeu tratamento de 15 Âl da soluÃÃo testada, que permaneceu em contato com o bloco por 60 segundos. ApÃs os tratamentos, amostras dentinÃrias foram removidas com emprego de lÃmina de bisturi e foram analisadas a partir da contagem de UFCs (unidades formadoras de colÃnias). Os experimentos foram realizados em triplicata e os dados, obtidos em UFCs foram convertidos em log base-10. Os testes estatÃsticos empregados foram anÃlise de variÃncia (ANOVA), seguida de Teste de Tukey. NÃo houve diferenÃa estatÃstica entre as concentraÃÃes de EGCG empregadas e a soluÃÃo salina (p > 0,05). AlÃm disso, nÃo houve diferenÃa estatÃstica entre as concentraÃÃes de EGCG (p > 0,05). No entanto, houve diferenÃa estatisticamente significativa entre a clorexidina e os demais grupos (p < 0,05). Conclui-se, a partir dos dados encontrados, que a substÃncia investigada nÃo deve ser empregada em preparos cavitÃrios com a finalidade de eliminaÃÃo de patÃgenos, visto que nÃo se mostrou eficaz como antimicrobiano nas concentraÃÃes testadas.
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Kafley, Suvash. "Distribution of catechins, epicatechins and methylxanthines in caffeinated and decaffeinated green tea." Online version, 2008. http://www.uwstout.edu/lib/thesis/2008/2008kafleys.pdf.
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Chiu, Wing-yee. "Effect of chronic green tea consumption on lipolysis in rats." Hong Kong : University of Hong Kong, 2002. http://sunzi.lib.hku.hk/hkuto/record.jsp?B25139393.
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Rogers, James L. "Major tea catechin inhibits dendritic cell maturation in response to microbial stimulation." [Tampa, Fla] : University of South Florida, 2007. http://purl.fcla.edu/usf/dc/et/SFE0002176.
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Cheng, Tak-him Terence. "Neuroprotective effect of green tea extracts." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/b40203517.
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Sirk, Timothy Wayne. "A Molecular Dynamics Study on the Interaction of Tea Catechins and Theaflavins with Biological Membranes." Diss., Virginia Tech, 2009. http://hdl.handle.net/10919/26946.
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Molecular dynamics simulations were performed to study the interactions of bioactive catechins and theaflavins commonly found in tea with lipid bilayers, as a model for cell membranes. Previously, multiple experimental studies rationalized the anticarcinogenic, antibacterial, and other beneficial effects of these compounds in terms of physicochemical molecular interactions with cell membranes. To contribute toward understanding the molecular role of tea polyphenols on the structure of cell membranes, simulation results are presented for seven catechins and three theaflavins in lipid bilayer systems which are both pure (POPC) and representative of HepG2 cancer cells (POPC and POPE). Our simulations show that the catechins and theaflavins evaluated have a strong affinity for the lipid bilayer \textit{via} hydrogen bonding to the bilayer surface, with many of the catechins able to penetrate beneath the surface. Epigallocatechin-gallate (EGCG) and Theaflavin-3,3'-digallate showed the strongest interaction with the lipid bilayers based on the number of hydrogen bonds formed with lipid headgroups. The simulations also provide insight into the functional characteristics of the tea compounds that distinguish them as effective compounds to potentially alter the lipid bilayer properties. The results on the hydrogen-bonding effects may contribute to a better understanding of proposed multiple molecular mechanisms of the action of catechins and theaflavins in microorganisms, cancer cells, and tissues.Ph. D.
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Harr, Jennifer C. "An electrophysiological study of the effects of resveratrol and catechin at GABAa receptors." Scholarly Commons, 2007. https://scholarlycommons.pacific.edu/uop_etds/649.
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Resveratrol and catechin have behavioral and neuroprotective effects that may be due to their interaction with neuronal ion channels. It was hypothesized that the grape compounds, resveratrol and catechin modulate GABAAA receptors. To address this hypothesis, the effects of resveratrol and catechin were investigated on human recombinant GABAA receptors expressed in HEK-293 cells using electrophysiological techniques.<.p>
HEK-293 cells were cultured and transfected using eDNA encoding human GABAA receptors. GABA-evoked currents were recorded from HEK cells 24-48 hours following transfection. Cells were voltage clamped in the whole cell configuration at -60mV using the patch-clamp technique. Ligand-activated currents were recorded and stored, using Win WCP software, on a desktop computer.
Resveratrol (1- 100μM) dose-dependently potentiated GABA-evoked currents recorded from α1β2< /sup>γ2 and α1β2 GABAA receptors. Resveratrol did not modulate a α1β2< /sup>γ2 and α1β2 GABAA receptors. Furthermore, resveratrol did not act through the benzodiazepine binding site. The low efficacy and subunit selectivity of resveratrol is a promising discovery for the development of a highly specific GABAergic modulator. Conversely, catechin (1-100αM) dose-dependently inhibited GABA-evoked currents recorded from α1β2 and α1β1 GABAA receptors. The degree of inhibition was the same for both receptor subtypes. Catechin did not modulate α1β2γ2 or α1β1γ2 GABAA receptors. The selectivity of catechin for receptors lacking the γ subunit is similar to the effects of zinc and did not involve the benzodiazephine site on GABAA receptors.
This study has shown that catechin and resveratrol are subunit-selective modulators of human GABAA receptors. These compounds could lead to the development of novel agents to be used in treating neurological disorders. These data support the use and study of natural products for the development of agents that act selectively on the nervous system.
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Gulu, Nontobeko Benhilda. "Functional and rheological properties of Bambara groundnut starch-catechin complex obtained by chemical grafting." Thesis, Cape Peninsula University of Technology, 2018. http://hdl.handle.net/20.500.11838/2806.
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Thesis (MTech (Food Technology))--Cape Peninsula University of Technology, 2018.The aim of this study was to produce Bambara groundnut (BGN) starch-catechin complex using chemical initiators (ascorbic acid and hydrogen peroxide) and cyclodextrin (alpha and beta) with the view to obtain a functional ingredient for the food industry. BGN starch was successfully extracted from BGN flour through dry milling method, yielding 32% of BGN starch. Native BGN starch was chemically modified using ascorbic acid (1% w/w) and hydrogen peroxide (165% w/w) as redox, biocompatible initiator for grafting catechin to the BGN starch. In addition, cyclodextrin (alpha and beta) were also used as initiators for modifying BGN starch through complexation methods. Complexation methods used included the microwave, co-evaporation and kneading. The characterization of native and modified BGN starches was carried out by performing scanning electron microscopy, powder X-ray diffraction, Fourier Transform Infrared (FTIR) and fluorescence spectroscopy analysis. Functional, thermal and rheological properties of native and modified BGN starches were evaluated. The pasting properties of BGN starches were determined using the Rapid Visco Analyser (RVA). According to the SEM profile, native BGN starch had round, oval and elliptical shapes typical for legume starches. Native BGN starch displayed a typical type-C crystallinity which is common among legumes with strong peaks at 2θ of 15o, 17o and 23o. BGN starches modified through complexation methods had sharper peaks indicating an increase in starch crystallinity; however, following chemical modification there was loss in starch crystallinity which was evidenced by the amorphous region in the chemically modified BGN starches. Structure of native and modified BGN starches was confirmed by FTIR. The FTIR spectra of native BGN starch showed variable peaks at 3285.34 cm-1, 2931.69 cm-1, 1634.36 cm-1, 1336.77 cm-1 which are attributed to OH stretching, C-H stretching, water bending vibrations and C-O stretching, respectively. Furthermore, the FTIR results confirmed that native BGN starch is made up of glucose molecules just like all other starches. All modified BGN starches displayed a new absorption peak at 1020 cm-1 wavelength, thus indicating that starch modification was successful. On the other hand, all BGN starch-catechin complexes displayed a new absorption peak in the range of 1520 -1560 cm-1, attributed to the C-C stretching within the aromatic ring of the catechin. The successful grafting of catechin to BGN starch was also confirmed by the fluorescence spectroscopy results, where all the BGN starch-catechin complexes had an emission peak at 320 nm while native BGN starch had an emission peak at 270 nm. Antioxidant capacity of BGN starch was determined through DPPH and ORAC antioxidant assays. Within the DPPH assay, the antioxidant activity ranged from 2.26 to 38.31 μmol TE/g. The antioxidant activity of modified BGN starch-catechin complexes was significantly (p ≤ 0.05) higher than the ones modified without catechin. On the other hand, within the ORAC assay, the antioxidant activity ranged from 0.07 to 126.71 μmol TE/g. As opposed to the results obtained in DPPH assay, the antioxidant activity of chemically modified BGN starch-catechin complexes was significantly (p ≤ 0.05) higher than that of complexed BGN starch-catechin complexes. Chemical modification significantly increased the swelling capacity of native BGN starch while complexation methods significantly reduced it.
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Tan, Susi. "Self-assembled nanocomplexes comprising of green tea catechin derivatives and protein drugs for cancer therapy." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/29859.
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The drug-to-carrier ratio has been a considerable issue in the design of a drug carrier, because the use of unreasonably high quantities of carrier can lead to problems associated with carrier toxicity, metabolism and elimination. However, if the carrier itself displays therapeutic effects, the drug-to-carrier ratio would no longer be a concern, and the delivery system should attain greater therapeutic effects from both the drug and the carrier. Epigallocatechin gallate (EGCG), a major ingredient of green tea, has been recognized as an attractive functional compound due to its various potential therapeutic effects, including anticancer effects. Herein we design the core-shell micellar nanocomplex (MNC) spontaneously constructed by self-assembly from the EGCG derivatives and proteins. This system achieved a greater anticancer effect in vitro and in vivo when loaded with an anticancer protein, as compared to the native protein or the carrier alone. This unique green tea-based MNC is the first nanoparticle drug delivery system that takes advantage of the beneficial bioactivities of EGCG.
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余詩德 and Sze-tak Yu. "Effects of Chinese green tea and tea catechins on lipolysis." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31969677.
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Reis, Bruna de Oliveira [UNESP]. "Influência de inibidores de proteases no potencial de degradação do colágeno proveniente da dentina sadia, esclerótica e afetada por cárie." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/151462.
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Objetivo: Avaliar a influência de inibidores de proteases no potencial de degradação do colágeno das dentina sadia, esclerótica e afetada por cárie. Materiais e métodos: Trinta e nove molares humanos foram utilizados, treze para cada condição dentinária. Três fatias foram obtidas de cada dente, cada uma imersa em diferentes soluções: 1) saliva artificial; 2) clorexidina 2%; 3) EGCG 0,5%. Após incubação nas soluções por 1h, amostras foram sujeitas à degradação enzimática pela colagenase derivada da Clostridium histolyticum. Propriedades mecânicas de nanodureza (HIT) e módulo de elasticidade (Er) dos três diferentes tipos de dentina foram mensuradas antes e após a degradação, bem como a resistência à tração do colágeno. Resultados do teste de resistência à tração e nanoindentação foram submetidos à ANOVA dois e três fatores para medidas repetidas, e pós-teste de Tukey (α=0,05). Resultados: Maiores valores de resistência à tração foram encontrados para dentina sadia, nos grupos controle (40,30 ± 21,38 MPa) e EGCG 0,5% (30,05 ± 19,67 MPa). Antes da degradação, maiores valores de HIT (0,237 ± 0,062 GPa) e Er (5,58 ± 1,75 GPa) foram encontrados para o grupo EGCG 0,5%, na dentina afetada por cárie. Após a degradação, grupo clorexidina 2% apresentou maiores valores de HIT e Er para dentinas sadia (0,134 ± 0,020 GPa e 3,57 ± 0,40 GPa) e esclerótica (0,201 ± 0,048 GPa e 4,30 ± 0,56 GPa). Conclusões: O uso da clorexidina 2%, principalmente em dentina esclerótica, mostrou-se mais efetivo em promover aumento na resistência à tração e nas propriedades mecânicas, antes e após a degradação. A EGCG 0,5% apresentou melhor efeito sobre as propriedades mecânicas na dentina afetada por cárie, especialmente antes da degradação enzimática. Relevância Clínica: O efetivo conhecimento do mecanismo de ação de inibidores de proteases em diferentes tipos de dentina poderia contribuir para melhoria da resistência do substrato e para maior longevidade dos processos de união sobre este tecido.
Objetive: To evaluate the influence of proteases inhibitors on the collagen degradation from sound, sclerotic and caries-affected dentin. Materials and Methods: Thirty-nine human molars were used, thirteen for each dentin condition. Three slices were obtained from each tooth, each one immersed in different solutions: 1) artificial saliva; 2) 2% chlorhexidine; 3) 0.5% EGCG. After incubation in the solutions for 1h, samples were subjected to enzymatic degradation by collagenase derived from Clostridium histolyticum. Mechanical properties of nanohardness (HIT) and elastic modulus (Er) of the three types of dentin were measured before and after degradation, as well as the microtensile strength. Results of the microtensile strength and nanoindentation tests were submitted to ANOVA two and three factors for repeated measurements, and Tukey post-test (α = 0.05). Results: Higher values of tensile strength were found for sound dentin in control (40.30 ± 21.38 MPa) and 0.5% EGCG (30.05 ± 19.67 MPa) groups. Before degradation, higher values of HIT (0.237 ± 0.062 GPa) and Er (5.58 ± 1.75 GPa) were found for the 0.5% EGCG group in caries-affected dentin. After degradation, 2% chlorhexidine group had higher values of HIT and Er for sound (0.134 ± 0.020 GPa and 3.57 ± 0.40 GPa) and sclerotic (0.201 ± 0.048 GPa and 4.30 ± 0.56 GPa) dentin. Conclusions: The use of 2% chlorhexidine, mainly in sclerotic dentin, was shown to be more effective in promoting increase in the microtensile strength and mechanical properties, before and after the degradation. The 0.5% EGCG showed a better effect on mechanical properties in caries-affected dentin, before the enzymatic degradation. Clinical Relevance: The effective knowledge of the mechanism of action of protease inhibitors in different types of dentin could contribute to the improvement of the resistance of the substrate and to the longer longevity of the bonding processes on this tissue.
FAPESP: 2015/10566-7
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Chen, Jie Jack, and 陳杰. "Growth inhibition effects of green tea and epigallocatechin gallate inbladder tumors." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B4257772X.
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BALASUBRAMANIAN, SHREEKRIPA. "DOSE AND VEHICLE EFFECTS ON THE PENETRATION RATE OF SELECTED PLANT POLYPHENOLS THROUGH HUMAN SKIN." University of Cincinnati / OhioLINK, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1016481382.
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Tanner, Stephan [Verfasser]. "Untersuchungen zu den molekularen und protektiven Wirkungen von Catechin und seinen Derivaten in Caenorhabditis elegans / Stephan Tanner." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2013. http://d-nb.info/1044680016/34.
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Kyejjusa, Yusuf. "Isolation And Characterisation Of Antioxidant Compounds In Yellow Rose Root Extracts." Master's thesis, METU, 2009. http://etd.lib.metu.edu.tr/upload/3/12610686/index.pdf.
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A phytochemical investigation on methanolic extract of roots of yellow rose led to
the isolation of a catechin gallate. The crude extract first underwent fractionation
using petroleum ether, chloroform, ethylacetate, butanol with water as solvents in
their respective order. The emerging solvent fractions were subjected to further
separation using lipophilic sephadex (LH-20), and silica gel column chromatography
to isolate pure compounds. Analytical thin layer chromatography (TLC) was used to
confirm the presence of a catechin in butanol fraction. Purified catechin compound
was subjected to 2,2-diphenyl-1-picrylhydrazyl (DPPH) experiment to determine its
Radical Scavenging Capacity, which was found quite promising. Chemical structure
of purified compound was established by using Nuclear Magnetic Resonance (NMR)
and Mass Spectrometry (MS) experiments.
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趙詠頤 and Wing-yee Chiu. "Effect of chronic green tea consumption on lipolysis in rats." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31970461.
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Kopaniszen, Malgorzata. "Protective effect of green tea polyphenols on dinitrobenzene sulphonicacid (DNBS)-induced colitis in mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687466.
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Pereira, Daniela Santos. "Efeito do antioxidante epigalocatequina-3-galato na perda óssea durante a periodontite induzida por ligadura em ratos. Análise por tomografia microcomputadorizada 2D e 3D e histomorfométrica." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-26042016-095806/.
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A doença periodontal é uma das doenças inflamatórias crônicas mais comuns que acometem a população. A grande destruição tecidual observada durante o seu desenvolvimento tem sido atribuída ao processo inflamatório exacerbado e ao desequilíbrio favorável à geração de espécies reativas de oxigênio em relação àcapacidade de defesa dos antioxidantes. A epigalocatequina-3-galato (EGCG) obtida da Camellia sinensis é uma substância que apresenta potencial antioxidante e antiinflamatório e, mais recentemente, testes in vitro têm mostrado que também possui atividade anti-osteoclastogênica, sendo apontada como uma possível droga para uso terapêutico nas patologias ósseas com excessiva atividade osteoclástica e destruição óssea. O objetivo do trabalho foi verificar morfométricamente em imagens obtidas pela tomografia microcomputadorizada (micro-CT) e cortes histológicos se a administração diária de EGCG reduz o processo inflamatório e a perda óssea alveolar na doença periodontal induzida por ligadura em ratos. O primeiro molar inferior direito de 60 ratos foi amarrado com fio de seda 3.0 e divididos em grupo sem tratamento (GST), grupo tratado com EGCG (GTEGCG) que recebeu diariamente por gavagem 100mg/Kg de EGCG e grupo Sham (GTsalina) que recebeu apenas solução salina. Nos períodos de 0, 7, 14 e 21 dias (n=5 animais/período/grupo) imagens digitais foram obtidas no microtomógrafo sendo submetidos à análise do nível ósseo periodontal (PBL) e da densidade óssea (BV/TV) inter-radicular. Nos cortes longitudinais do M1 corados pela HE foi avaliado o PBL e morfometricamente o percentual e volume de processo inflamatório e tecido ósseo, além do número osteoclastos/cm2. Os dados foram submetidos à ANOVA a dois critérios e ao teste de Tukey (p<0,05). O PBL determinado nas imagens microtomográficas e histológicas mostraram que a perda óssea aumenta em todos os grupos durante a fase aguda da doença (0 a 14 dias) e estabiliza na fase crônica (14 dias-21 dias). Em geral, o PBL foi menor no GTEGCG (média de 0,839 mm) comparado aos GST e GTsalina (média de 0,953 ). Quanto à densidade óssea o BV/TV foi maior no GTEGCG (68%) comparados aos GST (62,06%). O percentual do processo inflamatório e o número de osteoclastos foram menores no GTEGCG, com pico aos 14 dias (3,4% de processo inflamatório e 32 osteoclastos/cm2), comparados aos GST e GTsalina cujo o pico foi aos 7 dias (média de 8,6% de processo inflamatório e 68 osteoclastos/cm2). Concluímos que, no modelo de periodontite induzida por ligadura, o tratamento com EGCG diminui o processo inflamatório e a osteoclastogênese e consequentemente a perda óssea e a severidade da doença.Periodontal disease is currently one of the most common chronic inflammatory diseases affecting the population. The large tissue destruction observed during its development, has been attributed to exacerbated inflammatory process and unbalance response between production of reactive oxygen species and antioxidant defense capacity. Recently, the substance epigallocatechin-3-gallate (EGCG) obtained from Camellia sinensis have been associated to antioxidant and antiinflammatory actions. In vitro studies have shown that EGCG has also antiosteoclastogenic activity suggesting to be a potencial drug for use in therapeutic treatment of bone diseases with excessive osteoclast formation and bone destruction. The aim of this study was to verify morphometrically in micro-ct and histological images whether daily administration of EGCG inhibits/decreases alveolar bone loss in periodontal disease induced in rats by ligature. The lower right first molar of 60 rats was tied with surgical suture thread 3.0. The animals were divided into untreated group (GST), EGCG treated group (GTEGCG) which received 100mg/kg of EGCG by gavage daily and Sham group (GT saline) which received saline solution only. In periods of 0, 7, 14 and 21 days (n=5 animals/period/group) digital images were obtained in microtomography (SkyScan1176) and subjected to analysis of PBL in the mesial, distal, buccal and lingual root and BV/TV bone volume percentage. In the sagittal slides PBL volumetric points and inflammatory process as well as the number of osteoclasts/cm2 was analyzed. Data were submitted to twoway ANOVA and Tukey test (p <0.05). PBL determined in microtomographic and histological images showed that bone loss increased and stabilized, respectively, in the all groups acute phase (days 0 to 14) and chronic phase (14 days, 21 days) of the disease. In general, the PBL was lower in GTEGCG (average 0,839 mm) compared to GST and GTsaline (average 0,953). Regarding bone density BV/TV in GTEGCG was higher (68%) compared to GST (62.06%). The percentage of inflammation and the number of osteoclasts was more mild in GTEGCG, reaching peak at 14 days (3.4% inflammatory process and 32 osteoclasts / cm2) compared to GST and GTsaline whose peak was at 7 days (average 8.6% inflammatory process and 68 osteoclasts / cm2). It was concluded that in the current model of periodontal disease induced by ligature, EGCG treatment decreases inflammatory process, osteoclastogenesis activity, bone loss, and consequently the severity of the disease.
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Yuskavage, Julia Kathryn. "Epigallocatechin Gallate in the Regulation of Insulin Secretion." Thesis, Virginia Tech, 2008. http://hdl.handle.net/10919/32761.
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In both Type 1 diabetes (T1D) and Type 2 diabetes (T2D), inadequate beta-cell mass and beta-cell dysfunction lead to impaired insulin secretion, and ultimately worsen glycemic control. Green tea has drawn wide attention due to its possible health-promoting properties, including enhancement of beta-cell function. We assessed the acute and relative long-term effects of epigallocatechin gallate (EGCG) on insulin secretion and synthesis from clonal beta-cells (INS1E cells), rat islets, and human islets, using 0.1, 1, or 5 µM. We determined if EGCG decreased blood glucose in healthy rats acutely, using 50 or 150 mg/kg body weight (BW), and after 12 days of supplementation in drinking water, using 0.1% and 0.5%. In the in vitro studies, EGCG significantly potentiated glucose-stimulated insulin secretion (GSIS) in rat islets (at 0.1, 1, and 5 µM) and human islets (at 1 µM), and elevated insulin content within INS1E cells (at 0.1, 1, and 5 µM) and human islets (at 1 µM), (P<0.05). Nutritional supplementation of EGCG (0.5% in drinking water) for 12 days in healthy rats significantly increased insulin synthesis, compared to that of controls, from 0.2 ± 0.02 to 1.4 ± 0.2 ng/mg protein, without alteration of insulin secretion in isolated islets (P<0.05). These findings demonstrate that EGCG may play a role in the regulation of pancreatic beta-cell function, thereby contributing to an anti-diabetic effect of this agent.Master of Science
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Rowley, Thomas John. "The Effect of Cocoa Flavanols on β-Cell Mass and Function." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6508.
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A hallmark of type 2 diabetes (T2D) is β-cell dysfunction and the eventual loss of functional β-cell mass. Therefore, mechanisms that improve or preserve β-cell function could be used to improve the quality of life of individuals with T2D. Studies have shown that monomeric, oligomeric and polymeric cocoa flavanols have different effects on obesity, insulin resistance and glucose tolerance. We hypothesized that these cocoa flavanols may have beneficial effects on β-cell function. INS-1 832/13 derived β-cells and primary rat islets cultured with a monomeric catechin-rich cocoa flavanol fraction demonstrated enhanced glucose-stimulated insulin secretion, while cells cultured with total cocoa extract, oligomeric, or polymeric procyanidin-rich fractions demonstrated no improvement. The increased glucose-stimulated insulin secretion in the presence of the monomeric catechin-rich fraction corresponded with enhanced mitochondrial respiration, suggesting improvements in β-cell fuel utilization. Mitochondrial complex III, IV and V components were upregulated after culture with the monomer-rich fraction, corresponding with increased cellular ATP production. The monomer-rich fraction improved cellular redox state and increased glutathione concentration, which corresponds with Nrf2 nuclear localization and expression of Nrf2 target genes, including NRF-1 and GABPA, essential genes for increasing mitochondrial function. We propose a model by which monomeric cocoa catechins improve the cellular redox state, resulting in Nrf2 nuclear migration and upregulation of genes critical for mitochondrial respiration, and, ultimately, enhanced glucose-stimulated insulin secretion and β-cell function. These results suggest a mechanism by which monomeric cocoa catechins exert their effects as an effective complementary strategy to benefit T2D patients.
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Li, Xiaoyun, and 李晓云. "A systematic review of the losing weight efficacy and safety of green tea catechins in slimming products." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B46940261.
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Haramizu, Satoshi. "Verification of the senescence-accelerated mouse as a model of aging-related physical performance decline and beneficial effects of catechins on physical performance." Kyoto University, 2014. http://hdl.handle.net/2433/193549.
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Sasaki, Geoffrey Y. "Dietary Green Tea to Attenuate Metabolic Endotoxemia-Associated Inflammation Along the Gut-Liver Axis." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1595278825258631.
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Ohyama, Kana. "Studies on the food compounds showing anti-obesity effect and their mechanism to suppress obesity." Kyoto University, 2016. http://hdl.handle.net/2433/217117.
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Rinaldo, Daniel [UNESP]. "Determinação de enantiômeros em extratos vegetais por cromatografia quiral e dicroísmo circular." Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/105773.
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rinaldo_d_dr_araiq.pdf: 1188120 bytes, checksum: 1e4f3603501a8b454e918390b4c81bce (MD5)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Este trabalho abordou a determinação quali e quantitativa de enantiômeros de catequinas em extratos e infusões das folhas de espécies do gênero Byrsonima (Malpighiaceae), tais como: B.basiloba, B. cocolobifolia, B. crassa, B. intermedia e B. verbascifolia. O trabalho descreve a determinação rápida e eficiente de catequina, ent- catequina, epicatequina e ent-epicatequina por cromatografia líquida de alta eficiência acoplada a detector de arranjo de fotodiodos e dicrísmo circular, usando coluna de fase estaconária quiral. O método possui alta seletividade e permite identificar inequivocadamente diastereômeros de catequinas em matrizes complexas como extratos vegetais, com limites de detecção (0,42 a 0,77 μg mL-1 ) e quantificação (1,27 a 2,32 μg mL-1 ) satisfatórios para as condições analisadas, e valores de precisão (0,3 to 4,8%) e exatidão (70,0 a 110,2%) recomendados pela ANVISA. Com exceção da espécie B. intermedia, quatro espécies do gênero apresentaram em seus extratos e infusões os diastereômeros catequina, epicatequina e ent-epicatequina. Experimentos para avaliar a epimerização da catequina indicaram que a incomum ent-epicatequina não é um artefato, podendo ser um produto do metabolismo de espécies do gênero Byrsonima. Enantiômeros da catequina apresentam diferentes atividades farmacológicas, o que pode causar a ocorrência de efeitos colaterais diversos, danosos à saúde humana. Portanto, esses resultados podem alertar quanto ao consumo indiscriminado de plantas medicinais pela população e contribuir para criação de políticas mais rigorosas no controle de qualidade de fitoterápicos no Brasil
This work deals with the qualitative and quantitative determination of catechin and epicatechin enantiomers both in extracts and infusions from the leaves of the Byrsonima (Malpighiaceae) species (B.basiloba, B. cocolobifolia, B. crassa, B. intermedia and B. verbascifolia). This work describes a simple and reliable analytical high performance liquid chromatographic (HPLC) method coupled with photodiode array detector and circular dichroism for simultaneous determination of catechin, ent-catechin, epicatechin and ent-epicatechin. The direct separation was obtained in normal phase by HPLC using chiral stationary phase. The method has high selectivity. Regardless of variations in retention time, it was possible to identify unequivocally the enantiomers of catechin and epicatechin in complex matrices like plant extracts with satisfactory limit of detection (0.42 to 0.77 μg mL-1 ) and limite of quantification (1.27 to 2.32 μg mL-1 ). Under the conditions used, precision values were 0.3 to 4.8%, whereas accuracy values were 75.0 to 110.2%, recommended by ANVISA. Aside from B. intermedia specie, the other four Byrsonima species presented catechin, epicatechin and ent-epicatechin diastereomers both in methanolic extract and infusions. Experiments were carried out for verification the possibility of catechin epimerization. It was observed that the unusual ent- epicatechin was not an artifact, but product of Byrsonima species metabolism. Enantiomers of catechin present dissimilar pharmacological activities, which may cause the occurrence of various side effects, harmful to human health. Therefore, these results may warn about the indiscriminate use of medicinal plants by the population and contribute to the quality control of Brazilian herbal medicines
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Rahman, Rosanna, and n/a. "Potential causes of the delayed neural damage observed post-stroke & the effects of epigallocatechin gallate administration." University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.122246.
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Stroke is the 3rd leading cause of death and the leading cause of major disability worldwide. Currently, there are no neuroprotective drugs approved for the acute treatment of ischaemic stroke. The vast majority of stroke therapeutics failed in clinical trials due to toxic side effects and/or a clinically irrelevant therapeutic window. This thesis is focused on exploiting the delayed neurodegeneration that occurs in the compromised penumbra, as these cells may be capable of being saved by therapeutic intervention in a clinically obtainable window. In order to investigate the ischaemic cascade and be able to draw conclusions that are applicable to humans, the international gold standard animal model for cerebral ischaemia, the filament insertion middle cerebral artery occlusion (MCAO) model, was established at the University of Otago. This model was validated under new laboratory conditions and employed adult male Sprague Dawley rats. After testing multiple occlusion lengths, it was concluded that a 2hr ischaemic period was sufficient to produce a consistent infarct of optimal size. It has been well documented that neuroinflammation contributes to much of the delayed progression of neural injury post-stroke. Therefore, the catechin (-)-epigallocatechin gallate (EGCG), which is an anti-inflammatory, anti-oxidant and free-radical scavenging agent was investigated in the MCAO model of stroke. 50mg/kg i.p. of EGCG or saline was administered immediately post-MCAO and animals were sacrificed at 72hr post-filament insertion. The results confirmed that treatment with EGCG was neuroprotective and non-toxic. However, EGCG also induced an over 50% increase in the risk of haemorrhagic conversions. The anti-platelet effects of EGCG and lack of toxicity suggests that the catechin may prove to be an efficacious prophylactic for stroke. The contrary findings for EGCG treatment led to the re-evaluation of the neuroinflammatory pathway for alternate mechanisms to target therapeutic interventions.
The temporal profile of the primary inducible enzymes nitric oxide synthase (NOS), cyclooxygenase (COX) and arginase (and their isoforms) were quantified 0, 3 and 7 days post-stroke. In both hemispheres, total NOS activity exhibited a significant and sustained up-regulation to 7 days post-occlusion. In the ipsilateral hemisphere at least half of the total increase was accounted for by inducible NOS (iNOS) expression. Arginase, which competes with NOS for L-arginine, demonstrated a delayed but significant increase in activity by day 7 in the infarcted hemisphere, thereby correlating well with the downward slope of NOS activity (illustrating the switch in the conversion pathway). COX activity was observably increased in the ipsilateral hemisphere, but the up-regulation did not reach significance by day 7. Alternately, the contralateral hemisphere displayed a significant decrease in activity by day 3. These results give conclusive evidence that the contralateral hemisphere is NOT an appropriate internal control and imply that NOS and COX inhibitors may prove to be efficacious for a much longer therapeutic window than current treatments. However, the delayed induction of COX activity may also indicate that this enzyme has a finite therapeutic window, as it may also stimulate remodelling of surviving neural networks. The prolonged up-regulation of inflammatory mediators implies that there may be an induction of an autoimmune component to the response. Therefore, the thymus (T) lymphocyte activation was quantified up to 14 days post-stroke. Cluster of differentiation (CD) 3⁺ T lymphocytes (equally contributed to by CD4⁺ and CD8⁺ T cells) exhibited a significant and sustained up-regulation in the infarcted region from day 3 up to at least day 14 post-ischaemia. Quantitative analysis of all cells present post-stroke determined that immune cells make up an average of 73% of all cells present in the 'peak' ischaemic areas. The CD4⁺ T helper cell response was delineated by double immunohistochemical labelling. Interferon-γ positively labelled with CD4⁺ T cells at days 3, 7 and 14 post-insult detailing a Th1-driven pro-inflammatory response. This evidence indicates that the autoimmune response is critical post-ischaemia and that it may be highly susceptible to modification by anti-inflammatory therapeutic intervention.
The primary downstream effect of the pro-inflammatory/immune cascade is apoptosis. The main organelle responsible for the 'go, no go' response to apoptotic factors is the mitochondria. In order to distinguish whether mitochondrial dysfunction was initiated shortly after ischaemia induction or if it was delayed, like the inflammatory/immune response, to a clinically relevant window, the temporal profile of mitochondrial complex inactivation was studied. It was found that mitochondrial membrane viability was impaired by day 3, followed by a significant decrease in respiratory complex activation and an increase in tissue injury by oxidative stress by 7 days post-ischaemia. These results indicate that targeting the early decrease in membrane viability or mitochondrial permeability transition pore opening combined with anti-apoptotic therapeutics, may attenuate the proceeding mitochondrial impairment in oxidative phosphorylation, reactive oxygen species generation and subsequent cell death cascades. The current investigations into the temporal profile and quantitative contributions of the inflammatory, immune and apoptotic mechanisms post-stroke highlight potential strategies for modulation by acute stroke therapeutics. Furthermore, the general knowledge amassed from these studies dictates the necessity of a new approach to therapeutic intervention. The acknowledgement of so many contributing systems suggests that in addition to a thrombolytic, a combination therapy involving multiple neuroprotectants should be employed to account for the multifaceted nature of the sequelae of ischaemic stroke.
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Teixeira, Maria Daniele Azevedo. "Efeito neuroprotetor da catequina e do estresse de imobilizaÃÃo subcrÃnico na DoenÃa de Parkinson experimental." Universidade Federal do CearÃ, 2011. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=5747.
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FundaÃÃo Cearense de Apoio ao Desenvolvimento Cientifico e TecnolÃgicoCoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
A DoenÃa de Parkinson (DP) à uma desordem neurodegenerativa caracterizada pela perda de neurÃnios dopaminÃrgicos na substancia nigra (SN). Estudos epidemiolÃgicos sugerem uma associaÃÃo entre estresse, depressÃo e DP. Agentes antioxidantes tem sido relatados como capazes de mudar o curso da doenÃa, bloqueando a neurodegeneraÃÃo dopaminÃrgica. Com a finalidade de estudar os efeitos neuroprotetores da catequina, um flavonÃide encontrado na Camelia sinensis, o presente trabalho avaliou os efeitos deste composto no comportamento motor, memÃria, avaliaÃÃo imunohistoquÃmica e bioquÃmica em um modelo de DP induzido em ratos pela 6-OHDA. Em uma outra etapa do trabalho tambÃm avaliou-se os efeitos da associaÃÃo do estresse com a DP sobre estes mesmos parÃmetros, usando um modelo animal de estresse de imobilizaÃÃo subcrÃnico (11d/6hrs). Os animais (ratos Wistar machos, 200-250g) foram tratados com catequina (10 e 30 mg/kg i.p.) diariamente por 16 dias, iniciando-se na ocasiÃo da lesÃo estriatal pela 6-OHDA (21Âg/ 3ÂL). Os resultados obtidos demonstram que a 6-OHDA aumentou o nÃmero de rotaÃÃes contralaterais à lesÃo induzida por apomorfina e a catequina nas duas doses foi capaz de reverter esse dano motor. Houve uma recuperaÃÃo da atividade exploratÃria e memÃria de trabalho promovido pela catequina nas doses testadas. A 6-OHDA diminuiu a imunorreatividade para tirosina hidroxilase (TH) e transportador de dopamina (DAT) no corpo estriado e mesencÃfalo, alÃm de promover uma diminuiÃÃo nos nÃveis de GSH. A catequina nas duas doses em animais lesionados pela 6-OHDA foi capaz de recuperar a imunorreatividade para TH e DAT, alÃm de aumentar significativamente os nÃveis de GSH em relaÃÃo aos animais lesionados pela 6-OHDA. A 6-OHDA promoveu a morte neuronal demonstrada pela diminuiÃÃo nos nÃveis de catecolaminas, a catequina, por sua vez, foi capaz de reverter esses nÃveis. O estresse de imobilizaÃÃo subcrÃnico nÃo reverteu o nÃmero de rotaÃÃes contralaterais induzidas pela apomorfina, nem melhorou a memÃria de trabalho dos danos pela 6-OHDA, mas foi capaz de melhorar a atividade locomotora e a memÃria aversiva. O estresse subcrÃnico levou os animais a um estado depressivo no teste de nado forÃado, o que nÃo foi observado em animais que sofreram apenas a lesÃo estriatal. Houve uma diminuiÃÃo no ganho de peso nos animais submetidos ao estresse. AlÃm disso, houve uma aumento discreto da imunorreatividade para a TH e DAT em animais submetidos ao estresse e lesÃo pela 6-OHDA. Em relaÃÃo Ãs catecolaminas, houve uma reversÃo parcial nos nÃveis de noradrenalina e serotonina pelo efeito do estresse. Os resultados do presente trabalho demonstram que tanto a catequina, quanto estresse de imobilizaÃÃo foram neuroprotetores neste modelo experimental da DP. A catequina na dose de 30mg demonstrou um efeito prÃ-oxidante. O estresse de imobilizaÃÃo parece ter exercido um condicionamento fisiolÃgico nos animais, protegendo, de certa maneira, dos efeitos tÃxicos da 6-OHDA.
Parkinsonâs disease (PD) is a neurodegenerative disorder reported since antiquity and characterized for neuronal dopaminergic loss mainly in the substantia nigra (SN). Epidemiological studies suggest association between depression and PD and stress has been implicated in causing depression. The currently available therapies can not prevent the progression of PD, but are able to contain the symptoms. Neuroprotective agents have been reported as able to change the course of the disease, stopping dopaminergic neurodegeneration. Many of these agents are derived from plants with antioxidant actions, as catechin, a flavonoid found in green tea. In order to study the neuroprotective effects of catechin, the present study evaluated the effects of this compound on motor behavior, memory, Immunohistochemistry, biochemical evaluation and determination of catecholamines in an animal model of PD by 6-OHDA. Another stage of the study also evaluated the effects of stress associated with PD on the same parameters, in an animal model of subchronic restraint stress (11d/6hrs). Animals (male Wistar rats, 200-250g) were treated with catechin (10 and 30mg/kg ip) daily for 16 days, starting at the time of injury by striatal 6-OHDA. Results show that 6-OHDA increased the number of rotations contralateral to the lesion induced by apomorphine and catechin in the two doses was able to reverse the 6-OHDA damage. There was a recovery of exploratory activity and working memory promoted by catechin in both doses. Catechin in a dose of 30mg worsened the aversive memory. 6-OHDA decreased the immunoreactivity for tyrosine hydroxylase (TH) and dopamine transporter (DAT) in striatum and midbrain, and promote a decrease in GSH levels. Catechin in two doses in animals injured by 6-OHDA was able to increase the immunoreactivity for TH and DAT, significantly increasing the levels of GSH compared to lesioned animals by 6-OHDA. 6-OHDA caused neuronal death demonstrated by decreasing levels of catecholamines, catechin, in turn, was able to reverse these levels. The subchronic restraint stress did not reverse the number of contralateral rotations induced by apomorphine, neither improved the working memory of the damage by 6-OHDA, but was able to increase the number of crossings and improve the aversive memory. Stressed subchronic animals led to an increase in immobilization time in the forced swimming test, which was not observed in animals that were only striatal injury. There was a decrease in weight gain in animals subjected to stress. There was a slight increase of immunoreactivity for TH and DAT in animals subjected to stress and injury by 6-OHDA. In relation to catecholamines, there was a partial reversal in the levels of noradrenaline and serotonin by the effect of stress. Results of this study demonstrate that both catechin and immobilization stress were neuroprotective in this experimental model of PD. The catechin in a dose of 30mg was both oxidant and pro-oxidant. Restraint stress appears to have exerted a priming in animals, protecting, in a way, the toxic effects of 6-OHDA.
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Zarella, Bruno Lara. "Efeito de resinas experimentais contendo inibidores de proteases da matriz sobre gelatinases e colagenases." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-14082013-094509/.
Full textAbstract:
A evolução das resinas compostas fez com que esses materiais passassem a ter uma durabilidade maior e características estéticas muito boas, mas o risco de cárie recorrente é ainda um problema a ser resolvido. Na tentativa de solucionar esse problema, estudos vêm sendo conduzidos na tentativa de se formularem resinas compostas contendo agentes antibacterianos, como é o caso da incorporação de clorexidina (CHX). Outro fato que impede a longevidade deste material é a degradação de matriz de colágeno por proteases ativadas por pH ácido. Para tentar contornar esse problema, a adição de clorexidina, assim como Epigallocatechin gallate (EGCg), clássicos antibacterianos e inibidores de proteases da matriz , como as metaloproteinases da matriz (MMP) a resinas, poderia melhorar a eficácia destes materiais como substitutos de dentina em procedimentos restauradores, aumentando a longevidade do tratamento restaurador, mediante preservação das propriedades mecânicas do material. Assim, o objetivo desse estudo é avaliar o poder de inibição de resinas experimentais contendo inibidores conhecidos de proteases da matriz sobre gelatinases e colagenase. Para isso, copolímeros experimentais foram preparados combinando Bis-GMA com o diluente TEGDMA (70/30 mol%). Com exceção do copolímero placebo (sem drogas), EGCg ou CHX foram incorporados a 1% em peso isoladamente ou em combinação, a 0,5% em peso cada. Amostras contendo EGCg, CHX ou EGCg e CHX concentradas 10X foram obtidas do armazenamento de espécimes polimerizados da resina experimental em água deionizada (1 mL) após o período de 24h a 37°C e sua posterior concentração. O efeito da ação dos inibidores foi checado por zimografia e confirmado por um ensaio enzimático específico para colagenases e gelatinases. Os dados passaram por teste de homogeneidade (Bartlett) e normalidade (Kolmogorov-Smirnov) e foram avaliados por ANOVA a 2 critérios, seguido pelo teste de Bonferroni para comparações individuais (p<0,05). Os resultados do presente estudo, mostraram que, in vitro, a liberação de EGCg e CHX incorporados em resinas é capaz de reduzir a atividade gelatinolítica das MMPs -2 e -9, bem como a atividade da colagenase bacteriana, sugerindo um efeito potencial no aumento da longevidade de restaurações de resinas. Com isso, podemos afirmar que a liberação de ativos de resinas experimentais é possível e que esses ativos são capazes de inibir as MMPs, assim sugerindo um novo substituto para dentina em procedimentos restauradores.The evolution of composite resins made these materials to have a greater durability and very good esthetics characteristics, but the risk of recurrent caries is still a problem to be solved. In the attempt to solve this problem, studies are being conducted with the purpose to formulate composite resins containing antibacterial agents, such as chlorhexidine (CHX). Another fact that prevents the longevity of this material is the degradation of the collagen matrix by the proteases activated by acidic pH. In order to solve this problem, the addition of chlorhexidine and/or Epigallocatechin gallate (EGCg), classical antibacterial agents and inhibitors of matrix proteases, such as matrix metalloproteinases (MMP) in resins, could improve the efficacy of these materials as dentin substitutes in restorative procedures, increasing the longevity of the restorative treatment, while preserving the mechanical properties of the material. Thus, the aim of this study is to evaluate the ability of experimental resins containing known matrix protease inhibitors on the inhibition of gelatinases and collagenase. For this purpose, experimental copolymers were prepared combining Bis-GMA with the diluent TEGDMA (70/30 mol%). Except for the placebo copolymer (drug free), EGCg or CHX were incorporated at 1% in weight, isolated or in combination (0.5% in weight each). Samples containing EGCg, CHX or EGCg and CHX concentrated 10X were obtained after storage of polymerized specimens of the experimental resin in deionized water (1 mL) after the period of 24 h, at 37°C and after that were concentra. The effect of the action of the inhibitors was checked by zymography and confirmed by an enzymatic test specific for collagenases and gelatinases. The data passed in the tests of homogeneity (Bartlett test) and normality (Kolmogorov-Smirnov test), and were evaluated by 2-way ANOVA, followed by Bonferroni test for individual comparisons (p<0.05). The results of this study showed that the in vitro release of EGCG and CHX incorporated in resins was able to reduce the gelatinolytic activity of MMPs-2 and -9 and bacterial collagenase activity, suggesting a potential effect in increasing the longevity of resin restorations. It can be concluded that the release of drugs from experimental resins is possible and that these drugs are able to inhibit MMPs, thereby suggesting a new substitute for dentin in restorative procedures.
41
Chen, Shu-Ping, and 陳淑萍. "Study on Antioxidant Activity of Catechin." Thesis, 2017. http://ndltd.ncl.edu.tw/handle/15977129546231031082.
Full textAbstract:
碩士國立中興大學
生命科學院碩士在職專班
105
Tea is a healthy way at home and abroad. It is considered a magical effect of herbs in ancient time, has become the daily drink for everyone. Studies have shown that tea has a significant effect on human health. The main organic compounds in tea are tea polyphenols. Polyphenols are strong antioxidant, with physiological activity and immune function in the body. Catechin is one of the important ingredients of polyphenols. It universal exist in tea, foods. Green tea is rich in catechins and also a source of bitterness in tea. The four main structures of catechins are (-)-epicatechin (EC), (-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG). Most of the previous studies were discussed for EGCG, relatively less than the other three structures. So this study will evaluate that antioxidant activity in a tube and cell test in vitro for EC, ECG, EGC, EGCG. Compare with the difference between the four in antioxidant activities and the degree of influence in the cell. At antioxidant activities, the results showed that the ability of scavenging DPPH free radicals of catechins four kinds of structures was not very different, and the low concentration had a good scavenging effect. In the superoxide anion scavenging project, results are expressed EGCG has the best clearance ability, while EC is the worst. ABTS free radical scavenging results show that ECG and EGCG had a similar clearance effect, EGC and EC are slightly worse. Cell test section, an intracellular ROS production test used high dose and reaction 24 hours condition. The results shown ECG, EGCG has the effect of significantly reducing ROS generation. EC and EGC have no difference. In cell viability, ECG and high concentration of EGC, EGCG were significantly different, representing three structures with the ability to kill cancer cells. Therefore, catechin effectively remove ROS and kill cancer cells to achieve anti-cancer effect. Overall, ECG has an advantage in scavenging oxides and free radicals. EC effectively removes free radicals, but on ROS generation was not affected. The antioxidant activity of four kinds of catechins was ECG > EGCG > EGC > EC. The four structures of catechins have high antioxidant activity, but have different scavenging effects of different classes of free radicals, especially in cell tests. For a single structure catechin antioxidant mechanism is necessary to further study, look forward to catechins in the treatment can be used with a single structures catechins to achieve more efficient use.
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Lee, Yueh Lin, and 李岳霖. "Pharmacokinetic study of (+)-Catechin in rabbits." Thesis, 1994. http://ndltd.ncl.edu.tw/handle/39482456003589472331.
Full textAbstract:
碩士台北醫學院
藥學研究所
82
(+)-Catechin(3,3',4',5,7-tetrahydroxyflavan)是屬於一種 flavonoid 之化合物,在植物界分佈廣泛,它具有顯著的肝保護作用.目前在歐洲臨床 上口服治療急性濾過性病毒肝炎,及避免肝毒性物質和酒精所引起之肝傷 害.本實驗除了對(+)-Catechin之分析方法及血液內之安定性再探討外並 選擇家兔為實驗動物,以不同途徑之投與方式,包括靜脈投與,腹膜腔內 (intraperitonael)投與以及口服投與,來觀察(+)-Catechin在家兔體內之 藥物動力學的表現, 進一步來探討(+)-Catechin在家兔體內之生體可用 率 (bioavaila- bility).本實驗所使用的分析方法採用固-液抽提 (solid-liquid extraction)的方式,使用aluminum oxide為抽提之物質, 並用螢光檢測器(fluorescence detector),增加分析之靈敏度,最低檢測 濃度可達10ng/ml.選擇八隻家兔靜脈注射三種不同劑量，15、20、30mg/ kg之 (+)-Catechin,在此劑量範圍下呈 Dose Independent之藥物動力學, 其數據處理過程符合二室模式,經由靜脈注射30mg/kg,腹膜腔內投與30mg/ kg與口服100mg/kg之(+)-Catechin於家兔體內的結果得知,其代謝屬於線 性藥物動力學(linear pharmacokinetic),而其生體可用率分別為0.85 ±0.36與 0.02±0.01,顯示(+)-Catechin經由肝門脈吸收後,其肝臟首渡 效應(first pass effct),即通過肝臟時只有15%的藥量會被代謝掉;而口 服投與較高劑量100mg/kg之(+)-Catechin,其生體可用率僅有2% ,其原因 可能是由於藥物在腸胃道時之吸收不佳或代謝太快所導致。 The naturally occurring flavanol,(+)-Catechin(3,3',4',5, 7-tetrahydroxyflavan),which is found widespread in plants has been used to traet acute viral hepatitis and prevent hepatic disorders induced by ethanol or hepatotoxic substance in Europe. Up to now, there were few reports about the phar- macokinetics of (+)-Catechin in human and animals reported. In present syudy, the pharmacokinetic of(+)-Catechin with different doses and administrative routes in rabbits was studied. In analytical study, aluminum oxide was used as solid phase extraction material in solid-liquid extraction process. After extraction, a reverse phase HPLC method with fluorescence detector was developed. Under this chromatogra- phic condition, good linearity of standard curve (range 20~ 8000ng/ml, r=0.9999) of (+)-Catechin was obtained and the detective limitation of (+)-Catechin was 10ng/ml. After three different doses of (+)-Catechin (15,20,30mg/kg), there were no significant differnces between elimination rate constant and dose of I.V. administrated. The AUC (area under curve) obtained from I.V. administration of (+)-Catechin was propor- tional to various doses. This means a dose independant phar- macokinetics of (+)-Catechin in rabbits(Y=1.1299X+3.9029, r=0.9585 p<0.001). The intraperitoneal(30mg/kg) and oral (100mg/kg) administration of (+)-Catechin also showed a linear pharmacokinetics. The bioavailability of intraperitoneal and oral administration were 0.85±0.36 and 0.02±0.01, respectively. This means about 15% of (+)-Catechin may be metabolized by liver(hepatic first pass effect), and the bioavailability of oral administration may result from poor absorption of (+)-Catechin in the gastro- intestinal tract.
43
"Antioxidative activities of green tea catechins (Jasmine tea)." 1999. http://library.cuhk.edu.hk/record=b6073186.
Full textAbstract:
Thesis (Ph.D.)--Chinese University of Hong Kong, 1999.Includes bibliographical references (p. 218-235).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
44
"Tea catechins: epimerization, antioxidant activity and effect on body fatness in rats." 2004. http://library.cuhk.edu.hk/record=b6073685.
Full textAbstract:
Xu Jinze."August 2004."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2004.
Includes bibliographical references (p. 165-182).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Mode of access: World Wide Web.
Abstracts in English and Chinese.
45
"Studies on the mechanisms and anti-tumor activities of green tea epicatechin isomers." 2000. http://library.cuhk.edu.hk/record=b5890404.
Full textAbstract:
by Ip Wai-Ki.Thesis (M.Phil.)--Chinese University of Hong Kong, 2000.
Includes bibliographical references (leaves 213-233).
Abstracts in English and Chinese.
ACKNOWLEDGEMENTS --- p.i
ABBREVIATIONS --- p.ii
ABSTRACT --- p.vi
撮要 --- p.x
TABLE OF CONTENTS --- p.xiv
Chapter CHAPTER 1: --- GENERAL INTRODUCTION
Chapter 1.1 --- Hematopoiesis --- p.1
Chapter 1.1.1 --- Introduction to Hematopoiesis --- p.1
Chapter 1.1.2 --- Cytokines in Hematopoiesis --- p.4
Chapter 1.2 --- Leukemia --- p.6
Chapter 1.2.1 --- Leukemia: Abnormalities in Blood Cell Formation --- p.6
Chapter 1.2.2 --- Classification of Leukemia --- p.8
Chapter 1.2.3 --- The Causes and Molecular Basis of Leukemia --- p.8
Chapter 1.2.4 --- Therapy of Leukemia --- p.11
Chapter 1.2.5 --- Control of Leukemia by Hematopoietic Growth Factors and Other Compounds --- p.12
Chapter 1.2.6 --- Molecular Control of Apoptosis and Cell Cycle in Leukemia --- p.13
Chapter 1.2.6.1 --- Regulation of Cell Cycle and Apoptosis by Genes and Regulatory Proteins --- p.14
Chapter 1.2.6.1.1 --- Cell Cycle --- p.14
Chapter 1.2.6.1.2 --- Apoptosis --- p.15
Chapter 1.2.6.2 --- Role of Apoptosis and Cell Cycle in the Development of Leukemia --- p.17
Chapter 1.3 --- Green Tea --- p.19
Chapter 1.3.1 --- Origin and Cultivation of Tea Plants --- p.19
Chapter 1.3.2 --- Classification and Manufacturing of Tea --- p.21
Chapter 1.3.3 --- The Chemistry of Tea --- p.22
Chapter 1.3.3.1 --- Chemical Composition of Tea --- p.22
Chapter 1.3.3.2 --- Separation and Purification of Green Tea Polyphenols --- p.27
Chapter 1.3.3.3 --- The Chemical Properties of Green Tea Polyphenols --- p.28
Chapter 1.3.4 --- Bioavailability and Pharmacokinetic of Green Tea Epicatechins --- p.28
Chapter 1.3.4.1 --- Human Studies --- p.29
Chapter 1.3.4.2 --- Animal Studies --- p.30
Chapter 1.3.5 --- Physiological and Pharmacological Activities of Green Tea Catechins --- p.31
Chapter 1.3.5.1 --- Anti-oxidative Activity --- p.32
Chapter 1.3.5.2 --- Hypocholesterolemic and Hypolipidemic Activity --- p.33
Chapter 1.3.5.3 --- Anti-inflammatory Activity --- p.34
Chapter 1.3.5.4 --- Anti-microbial Activity --- p.35
Chapter 1.3.5.5 --- Anti-mutagenic Activity --- p.36
Chapter 1.3.5.6 --- Anti-carcinogenesis --- p.37
Chapter 1.3.5.7 --- Direct Anti-tumor Activity --- p.41
Chapter 1.3.5.8 --- Modulating Activity in Endocrine System --- p.43
Chapter 1.3.5.9 --- Other Biological Activities --- p.43
Chapter 1.3.6 --- Possible Anti-cancer Mechanisms of Green Tea Epicatechins --- p.44
Chapter 1.3.6.1 --- Modulation of Anti-tumor Immunity --- p.44
Chapter 1.3.6.2 --- Direct Growth Inhibition by Controlling the Signal Transduction Pathways --- p.45
Chapter 1.3.6.3 --- Induction of Apoptosis and Cell Cycle Arrest --- p.46
Chapter 1.3.6.4 --- Inhibition of Tumor Metastasis --- p.47
Chapter 1.4 --- Aims and Scopes of This Investigation --- p.48
Chapter CHAPTER 2: --- MATERIALS AND METHODS
Chapter 2.1 --- Materials --- p.50
Chapter 2.1.1 --- Animals --- p.50
Chapter 2.1.2 --- Cell Lines --- p.50
Chapter 2.1.3 --- Sheep Red Blood Cells (SRBC) --- p.52
Chapter 2.1.4 --- "Cell Culture Medium, Buffers and Reagents" --- p.52
Chapter 2.1.5 --- Tea Extracts and Green Tea Epicatechins --- p.56
Chapter 2.1.6 --- Recombinant Cytokines --- p.57
Chapter 2.1.7 --- Vitamin Analogs --- p.59
Chapter 2.1.8 --- Taxol (Baccatin III N-benzoyl-β-phenyllisoserine ester) --- p.59
Chapter 2.1.9 --- 18β-Glycyrrhetinic Acid (18β-GA) --- p.60
Chapter 2.1.10 --- [methyl-3H] Thymidine (3H-TdR) --- p.60
Chapter 2.1.11 --- Liquid Scintillation Cocktail --- p.60
Chapter 2.1.12 --- Reagents and Buffers for Flow Cytometery --- p.61
Chapter 2.1.13 --- Reagents for DNA Extraction --- p.62
Chapter 2.1.14 --- Reagents for Total RNA Isolation --- p.63
Chapter 2.1.15 --- Reagents and Buffers for RT-PCR Study --- p.64
Chapter 2.1.16 --- Reagents and Buffers for Gel Electrophoresis --- p.67
Chapter 2.1.17 --- Reagents and Buffers for Western Blot Analysis --- p.68
Chapter 2.2 --- Methods --- p.77
Chapter 2.2.1 --- Culture of the Leukemic Cell Lines --- p.77
Chapter 2.2.2 --- "Isolation, Preparation and Culture of Primary Mouse Cells" --- p.77
Chapter 2.2.3 --- Determination of Cell Viability --- p.78
Chapter 2.2.4 --- [3H]-TdR Incorporation Assay --- p.79
Chapter 2.2.5 --- Cell Morphology Study --- p.79
Chapter 2.2.6 --- Apoptosis Study --- p.80
Chapter 2.2.7 --- Animal Studies --- p.81
Chapter 2.2.8 --- Gene Expression Study --- p.82
Chapter 2.2.9 --- Protein Expression Study --- p.85
Chapter 2.2.10 --- Statistical Analysis --- p.88
Chapter CHAPTER 3: --- THE ANTI-TUMOR ACTIVITIES OF TEA EXTRACTS AND PURIFIED GREEN TEA EPICATECHIN ISOMERS ON VARIOUS LEUKEMIC CELL LINES
Chapter 3.1 --- Introduction --- p.89
Chapter 3.2 --- Results --- p.91
Chapter 3.2.1 --- The Effects of Tea Extracts on Various Leukemia Cells --- p.91
Chapter 3.2.1.1 --- Differential Anti-proliferative Effect of Different Tea Extracts on Various Leukemic Cell Lines In Vitro --- p.91
Chapter 3.2.1.2 --- Differential Cytotoxic Effect of Different Tea Extracts on the Murine Lymphocytic Leukemia L1210 Cells In Vitro --- p.92
Chapter 3.2.1.3 --- Induction of Apoptosis in HL-60 Cells by Different Tea Extracts In Vitro --- p.92
Chapter 3.2.2 --- The Effects of Purified Green Tea Epicatechin Isomers on Various Leukemic Cell Lines --- p.101
Chapter 3.2.2.1 --- In Vitro Anti-proliferative Effect of Green Tea Epicatechin Isomers on Various Human and Murine Leukemic Cell Lines --- p.101
Chapter 3.2.2.2 --- In Vitro Cytotoxic Effect of Green Tea Epicatechin Isomers on Various Human and Murine Leukemic Cell Lines --- p.117
Chapter 3.2.2.3 --- Effects of Green Tea Epicatechin Isomers on the Differentiation of Myeloid Leukemia Cells --- p.131
Chapter 3.2.2.4 --- Apoptosis-Inducing Effect of Different Green Tea Epicatechin Isomers on HL-60 and JCS Cells --- p.134
Chapter 3.2.2.5 --- Effect of EGCG on the In Vivo Tumorigenicity of Leukemia JCS and L1210 Cells --- p.142
Chapter 3.3 --- Discussion --- p.144
Chapter CHAPTER 4: --- MECHANISTIC STUDIES ON THE ANTI PROLIFERATIVE AND APOPTOSIS-INDUCING ACTIVITIES OF GREEN TEA EPICATECHIN ISOMERS ON LEUKEMIA CELLS
Chapter 4.1 --- Introduction --- p.149
Chapter 4.2 --- Results --- p.152
Chapter 4.2.1 --- Combining Effect of EGCG and Physiological Differentiation Inducers on the Proliferation of HL-60 and JCS Cells --- p.152
Chapter 4.2.2 --- Combining Effect of EGCG and Cytokines on the Proliferation of JCS Cells --- p.155
Chapter 4.2.3 --- Combining Effect ofEGCG and Other Phytochemicals on the Proliferation of HL-60 and JCS Cells --- p.161
Chapter 4.2.4 --- Modulatory Effect of EGCG on the Expression of Apoptosis-regulatory Genes in HL-60 Cells --- p.168
Chapter 4.2.5 --- Modulatory Effect of EGCG on the Expression of Growth-related and Apoptosis-regulatory Proteins in HL-60 Cells --- p.170
Chapter 4.3 --- Discussion --- p.177
Chapter CHAPTER 5: --- EFFECTS OF GREEN TEA EPICATECHIN ISOMERS ON THE GROWTH AND DIFFERENTIATION OF MURINE HEMATOPOIETIC CELLS
Chapter 5.1 --- Introduction --- p.184
Chapter 5.2 --- Results --- p.186
Chapter 5.2.1 --- In Vitro Effects of EGCG on Murine Lymphocytes --- p.186
Chapter 5.2.1.1 --- In Vitro Effect of EGCG on the Proliferation of Murine Splenocytes --- p.186
Chapter 5.2.1.2 --- In Vitro Effect of EGCG on the Mitogen-induced Proliferation of Murine Splenocytes --- p.186
Chapter 5.2.1.3 --- Cytotoxic Effect of EGCG on Murine Lymphocytes --- p.189
Chapter 5.2.2 --- Primary Humoral Immune Response to SRBCin EGCG-treated Mice --- p.191
Chapter 5.2.3 --- In Vitro Studies of the Effects of EGCG on Murine Bone Marrow Cells --- p.192
Chapter 5.2.3.1 --- Effects of EGCG on the In Vitro Proliferation of Murine Bone Marrow Cells --- p.192
Chapter 5.2.3.2 --- The Combining Effect of EGCG and Growth Factors on the In Vitro Proliferation of Murine Bone Marrow Cells --- p.192
Chapter 5.2.3.3 --- In Vitro Cytotoxic Effect of EGCG on Murine Bone Marrow Cells --- p.196
Chapter 5.2.4 --- Effect of EGCG on the Differentiation of Murine Bone Marrow Cells --- p.199
Chapter 5.2.5 --- Combining Effects of EGCG and Growth Factors on the Morphology of Murine Bone Marrow Cells --- p.199
Chapter 5.3 --- Discussion --- p.204
Chapter CHAPTER 6: --- CONCLUSIONS AND FUTURE PERSPECTIVES --- p.207
REFERENCES --- p.213
46
"The antioxidative and hypolipidemic activities of tea catechins." 1997. http://library.cuhk.edu.hk/record=b5889150.
Full textAbstract:
by Chan Ping Tim Timothy.Thesis (M.Phil.)--Chinese University of Hong Kong, 1997.
Includes bibliographical references (leaves 129-141).
ACKNOWLEDGMENTS --- p.I
ABSTRACT --- p.II
LIST OF ABBREVIATIONS --- p.IV
TABLE OF CONTENTS --- p.VI
Chapter CHAPTER 1 --- GENERAL INTRODUCTION --- p.1
Chapter 1.1 --- History of tea --- p.1
Chapter 1.2 --- Botany and agriculture of tea --- p.1
Chapter 1.3 --- Classification of tea --- p.2
Chapter 1.4 --- Composition of tea --- p.4
Chapter 1.5 --- Tea processing --- p.8
Chapter 1.5.1 --- Manufacture of green tea --- p.8
Chapter 1.5.2 --- Manufacture of black tea --- p.8
Chapter 1.5.3 --- Manufacture of oolong tea --- p.10
Chapter 1.6 --- Pharmacological effects of tea catechins --- p.13
Chapter 1.6.1 --- Antioxidative activity --- p.13
Chapter 1.6.2 --- Hypolipidemic activity --- p.14
Chapter 1.6.3 --- Antimutagenic activity --- p.15
Chapter 1.6.4 --- Anticarcinogenic activity --- p.15
Chapter 1.6.5 --- Antibacterial activity --- p.16
Chapter CHAPTER 2 --- ANTIOXIDATIVE ACTIVITIES OF TEA ETHANOL EXTRACTS AND GTC ON OXIDATION OF CANOLA OIL --- p.18
Chapter 2.1 --- Introduction --- p.18
Chapter 2.1.1 --- Lipid oxidation in food --- p.18
Chapter 2.1.2 --- Phenolic antioxidants --- p.19
Chapter 2.1.2.1 --- Major phenolic antioxidants used in food --- p.19
Chapter 2.1.2.2 --- Mechanism of action of phenolic antioxidants --- p.20
Chapter 2.1.2.3 --- BHA and its safety --- p.22
Chapter 2.1.2.4 --- BHT and its safety --- p.24
Chapter 2.1.3 --- Natural antioxidants --- p.24
Chapter 2.2 --- Objectives --- p.26
Chapter 2.3 --- Materials --- p.28
Chapter 2.4 --- Methods --- p.28
Chapter 2.4.1 --- GTC extraction --- p.28
Chapter 2.4.2 --- "HPLC analysis of GTC," --- p.29
Chapter 2.4.3 --- Isolation and purification of individual epicatechin isomers --- p.30
Chapter 2.4.4 --- Ethanol extraction of tea --- p.30
Chapter 2.4.5 --- Effect of tea ethanol extracts on oxygen consumption of canola --- p.31
Chapter 2.4.6 --- Effect of GTC on oxygen consumption of canola oil --- p.32
Chapter 2.4.7 --- Fatty acid analysis --- p.32
Chapter 2.4.8 --- Thermal loss of BHT --- p.33
Chapter 2.4.9 --- Thermal loss of GTC --- p.33
Chapter 2.4.10 --- Statistics --- p.35
Chapter 2.5 --- Results --- p.37
Chapter 2.5.1 --- Antioxidative activities of tea ethanol extracts --- p.37
Chapter 2.5.2 --- The yield and composition of GTC from jasmine tea --- p.51
Chapter 2.5.3 --- Antioxidative activity of GTC --- p.55
Chapter 2.5.4 --- Antioxidative activities of individual epicatechin isomers --- p.55
Chapter 2.5.5 --- Thermal loss of GTC --- p.60
Chapter 2.6 --- Discussion --- p.62
Chapter 2.6.1 --- Contribution of catechins to the antioxidative effects of tea ethanol extracts --- p.62
Chapter 2.6.2 --- Antioxidaitve activities of different types of teas --- p.62
Chapter 2.6.3 --- Proposed mechanisms for the relative activity of epicatechin isomers --- p.63
Chapter 2.6.4 --- Loss of BHT via volatilization --- p.66
Chapter 2.6.5 --- Potential of tea catechins as food antioxidants --- p.67
Chapter 2.6.5.1 --- Safety of GTC --- p.67
Chapter 2.6.5.2 --- Solubility of GTC --- p.68
Chapter 2.6.5.3 --- Effects of GTC on food quality --- p.68
Chapter CHAPTER 3 --- INHIBITORY EFFECTS OF GTC AND EPICATECHIN ISOMERS ON IN VITRO CU2+-MEDIATED LDL OXIDATION --- p.70
Chapter 3.1 --- Introduction --- p.70
Chapter 3.1.1 --- Mechanisms of LDL oxidation --- p.71
Chapter 3.1.1.1 --- Nature and sources of oxidants underlying LDL oxidation --- p.71
Chapter 3.1.1.2 --- Structural changes of ox-LDL --- p.72
Chapter 3.1.2 --- Biological effects of ox-LDL --- p.74
Chapter 3.1.3 --- Antioxidants and atherosclerosis --- p.76
Chapter 3.2 --- Objectives --- p.78
Chapter 3.3 --- Materials and methods --- p.79
Chapter 3.3.1 --- LDL isolation --- p.79
Chapter 3.3.2 --- LDL oxidation --- p.79
Chapter 3.3.3 --- Thiobarbituric acid-reactive substance (TBARS) assay --- p.80
Chapter 3.3.4 --- Lipid analysis --- p.80
Chapter 3.3.5 --- Statistics --- p.81
Chapter 3.4 --- Results --- p.82
Chapter 3.4.1 --- Protective effects of GTC against LDL oxidation --- p.82
Chapter 3.4.2 --- Varying protective effects of individual epicatechin isomers --- p.82
Chapter 3.4.3 --- Protective effects of GTC against oxidative degradation of PUFAs in LDL --- p.86
Chapter 3.5 --- Discussion --- p.88
Chapter 3.5.1 --- Tea catechins as anti-atherogenic agents --- p.88
Chapter 3.5.2 --- Mechanisms of the protective effects of tea catechins against Cu2+-induced LDL oxidation --- p.88
Chapter 3.5.3 --- Relative antioxidative activities of epicatchin isomers --- p.89
Chapter 3.5.4 --- Absorption of tea catechins --- p.90
Chapter 3.5.5 --- Pro-oxidant activities of tea catechins --- p.91
Chapter CHAPTER 4 --- HYPOLIPIDEMIC ACTIVITY OF GTC --- p.93
Chapter 4.1 --- Introduction --- p.93
Chapter 4.1.1 --- High serum cholesterol as a risk factor of CHD --- p.93
Chapter 4.1.2 --- Serum TG and CHD --- p.94
Chapter 4.1.3 --- Hypolipidemic effect of tea --- p.95
Chapter 4.1.4 --- Hamster as an animal model of cholesterol metabolism --- p.96
Chapter 4.2 --- Objectives --- p.97
Chapter 4.3 --- Materials and methods --- p.98
Chapter 4.3.1 --- Animals --- p.98
Chapter 4.3.2 --- Experiment 1 --- p.98
Chapter 4.3.3 --- Experiment 2 --- p.100
Chapter 4.3.4 --- Experiment 3 --- p.101
Chapter 4.3.5 --- "Serum lipid, lipoprotein and apolipoprotein determinations" --- p.101
Chapter 4.3.6 --- Lipid analysis of liver and carcass --- p.102
Chapter 4.3.7 --- Analysis of fecal lipid content --- p.102
Chapter 4.3.8 --- Determination of hepatic cholesterol content --- p.103
Chapter 4.3.9 --- Assay of fatty acid synthase activity --- p.105
Chapter 4.3.10 --- Statistics --- p.105
Chapter 4.4 --- Results --- p.106
Chapter 4.4.1 --- Growth and food intake --- p.106
Chapter 4.4.2 --- Effects of different levels of dietary GTC on serum TG and cholesterol --- p.106
Chapter 4.4.3 --- Time course study of the hypolipidemic effects of dietary GTC --- p.109
Chapter 4.4.4 --- Effects of GTWE on serum lipid and apolipoprotein profiles --- p.113
Chapter 4.4.5 --- "Effects of dietary GTC on hepatic TG, FFA and cholesterol contents" --- p.113
Chapter 4.4.6 --- "Effects of dietary GTC on carcass TG, FFA and cholesterol contents" --- p.118
Chapter 4.4.7 --- Effects of dietary GTC on fatty acid synthase activity --- p.118
Chapter 4.4.8 --- Effects of dietary GTC on fecal lipids content --- p.118
Chapter 4.5 --- Discussion --- p.120
Chapter 4.5.1 --- Hypolipidemic effect of GTC --- p.120
Chapter 4.5.2 --- Effects of GTC on serum apolipoproteins --- p.120
Chapter 4.5.3 --- Implication of GTC intake in humans --- p.121
Chapter 4.5.4 --- Mechanisms for the hypolipidemic activity of GTC --- p.122
Chapter 4.5.5 --- Reduction in hepatic TG and FFA contents in GTC-fed hamsters --- p.123
Chapter 4.5.6 --- Suppression of body lipid accumulation by dietary GTC --- p.124
Chapter 4.5.7 --- Mechanisms for the hypocholesterolemic activity of GTC --- p.124
Chapter CHAPTER 5 --- CONCLUSIONS --- p.126
REFERENCES --- p.129
47
Yang, Shu-min, and 楊舒閔. "Control release of (+)-catechin from liposome by ultrasound." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/96388714155020036161.
Full textAbstract:
碩士義守大學
材料科學與工程學系碩士班
96
Tea polyphenols exist in the leaves of tea, and their functions are at the tumor’s cancerchemoprevention. Particularly in the antioxidative effects, anticarcinogenesis, and antiinflammatio. The characteristic of the Catechins in the polyphenol is the strong antioxidative ability. Because the lower bioavailability of Catechins, the metabolism and excretion only take 24 hours for human. This study focus on the application of Ca-free-EDTA Ringers’ solution and liposome for overcoming the lower bioavailability and the development of the Pluronic as the phosphlipid ultrasonic sensitivity tool. We explained the releasing efficiency of the content inside the liposome by different Pluronic and intensity of ultrasonic power. We wish to the relationship of the ultrasound, phospholipid, and Pluronic further. The stability of the Catechins could keep more then 90 days at 4℃ in the pH 5.0 Ca-free-EDTA Ringer’ s solution. The structure of the Catechins did not destroy by the ultrasound with the setup of 28 kHz frequency and 60 Watt. When the phospholipid bilayer absorbed F127,P105, and F108, the incorporated degree into the bilayer was F127＞P105＞F108.
48
盧威良. "Exploring the surface-enhanced raman scattering about catechin." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/53009654064822992986.
Full textAbstract:
碩士國立嘉義大學
應用化學系研究所
94
Abstract Surface enhanced Raman scattering (SERS) was used to investigate about the dye molecular before. In recent years, this technique applied to biological compounds gradually, such as protein, enzyme. In this study we investigated the catechin molecular at different pH and salts about the SERS effect, catechin have exist in many natures, and it’s a well antioxidant compound, however, catechin in both water and alcohol phase will have fluorescence interference, and difficult to measure the conventional Raman signal. At first, synthesis provided with different dimension silver nanoparticles combine with catechin, excitation wavelength 514.5nm (Argon ion laser), scattering light was collected by multichannel detection Charge-Coupled Devices (CCD), to measure the SERS signal, compare with different situation ( different salts, pH ), spectrum possess obviously difference, and bromide ion have the best inference in SERS signal, we also take advantage of UV spectrum in this study to observe diversification of compound with different situation. SERS have been developing about 40 years, this study not only more come to understand SERS but also expand the application and expansion of conventional Raman.
49
"Pharmacokinetics of tea catechins in the rat." 2001. http://library.cuhk.edu.hk/record=b5890905.
Full textAbstract:
Chen Yu.Thesis submitted in: November 2001.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2001.
Includes bibliographical references (leaves 98-112).
Abstracts in English and Chinese.
Acknowledgements --- p.I
List of publications --- p.II
Abstract --- p.III
Abstract (Chinese) --- p.IV
Abbreviations --- p.V
Chapter Chapter 1 --- Introduction --- p.1
Chapter 1.1 --- Tea --- p.1
Chapter 1.2 --- Green tea --- p.3
Chapter a) --- Chemical composition of green tea --- p.3
Chapter b) --- Pharmacological activities of green tea polyphenols --- p.6
Chapter c) --- Pharmacokinetics of green tea polyphenols --- p.10
Chapter 1.3 --- Objective --- p.14
Chapter Chapter 2 --- Validation of analysis method for tea catechins --- p.15
Chapter 2.1 --- Materials and methods --- p.16
Chapter a) --- Preparation of a catechin-mixture from tea --- p.16
Chapter b) --- Preparation of stock solutions --- p.18
Chapter c) --- Preparation of biofluid samples --- p.18
Chapter d) --- HPLC analysis of tea catechins --- p.19
Chapter 2.2 --- Results --- p.21
Chapter a) --- Catechin-mixture (tea extracts) --- p.21
Chapter b) --- "Extraction from plasma, urine and feces" --- p.21
Chapter c) --- HPLC analysis of biofluid samples --- p.23
Chapter 2.4 --- Discussion --- p.26
Chapter Chapter 3 --- Pharmacokinetics of tea catechins following administration of different doses of the catechin-mixture --- p.32
Chapter 3.1 --- Materials and methods --- p.33
Chapter a) --- Surgery and animal maintenance --- p.33
Chapter b) --- Dosing and sample collection --- p.33
Chapter c) --- Pharmacokinetics analysis of tea catechins --- p.35
Chapter 3.2 --- Results --- p.36
Chapter 3.3 --- Discussion --- p.50
Chapter Chapter 4 --- Pharmacokinetics of tea catechins following administration of different doses of individual catechins --- p.52
Chapter 4.1 --- Materials and methods --- p.53
Chapter a) --- Chemicals and reagents --- p.53
Chapter b) --- Pharmacokinetic study of tea catechins and the HPLC analysis --- p.53
Chapter c) --- Pharmacokinetic analysis of tea catechins --- p.54
Chapter 4.2 --- Results --- p.55
Chapter 4.3 --- Discussion --- p.67
Chapter Chapter 5 --- Plasma protein binding of tea catechins --- p.69
Chapter 5.1 --- Introduction --- p.69
Chapter 5.2 --- Materials and methods --- p.72
Chapter a) --- Ultrafiltration --- p.72
Chapter b) --- Preparation of stock solution --- p.73
Chapter c) --- Determination of nonspecific binding of the catechins --- p.73
Chapter d) --- Determination of ultrafiltration conditions --- p.74
Chapter e) --- In vitro plasma protein binding assay --- p.74
Chapter f) --- Statistical analysis --- p.75
Chapter 5.3 --- Results --- p.76
Chapter a) --- Nonspecific binding in ultrafiltration --- p.76
Chapter b) --- Protein binding of the catechins --- p.76
Chapter c) --- Statistical analysis --- p.76
Chapter 5.4 --- Discussion --- p.80
Chapter Chapter 6 --- Partition of tea catechins in red blood cell --- p.82
Chapter 6.1 --- Materials and methods --- p.83
Chapter a) --- Prepare of stock solution --- p.83
Chapter b) --- In-vitro erythrocyte partition --- p.83
Chapter c) --- Data Analysis --- p.83
Chapter 6.2 --- Results --- p.85
Chapter a) --- Selection of experiment conditions --- p.85
Chapter b) --- Partition of catechins to RBC --- p.85
Chapter 6.3 --- Discussion --- p.87
Chapter Chapter 7 --- Comparison of pharmacokinetics of tea catechins in mixture form versus pure compound --- p.89
Chapter Chapter 8 --- Conclusion --- p.95
References --- p.98
50
"Studies on the immunomodulatory and anti-tumour activities of green tea catechins." 1999. http://library.cuhk.edu.hk/record=b5889879.
Full textAbstract:
by Tung Kai Chiu.Thesis (M.Phil.)--Chinese University of Hong Kong, 1999.
Includes bibliographical references (leaves 152-166).
Abstracts in English and Chinese.
STATEMENT --- p.i
ACKNOWLEDGEMENTS --- p.ii
ABBREVIATIONS --- p.iv
ABSTRACT --- p.vii
撮要 --- p.x
TABLE OF CONTENTS --- p.xiii
Chapter CHAPTER 1: --- GENERAL INTRODUCTION
Chapter 1.1 --- AN OVERVIEW OF THE IMMUNE SYSTEM --- p.1
Chapter 1.1.1 --- Innate Immunity --- p.1
Chapter 1.1.2 --- Specific Acquired Immunity --- p.4
Chapter 1.2 --- IMMUNE RESPONSE TO TUMOURS --- p.7
Chapter 1.2.1 --- Specific Mechanisms --- p.7
Chapter 1.2.1.1 --- Cellular Immune Response --- p.7
Chapter 1.2.1.2 --- Humoral Immune Response --- p.9
Chapter 1.2.2 --- Non-specific Mechanism --- p.10
Chapter 1.2.2.1 --- Natural Killer Cells --- p.10
Chapter 1.2.2.2 --- Lymphokine-activated Cells --- p.11
Chapter 1.2.2.3 --- Tumour Infiltrating Lymphocytes --- p.12
Chapter 1.2.2.4 --- Macrophages --- p.13
Chapter 1.2.2.5 --- Other Cell Types Mediating Non-specific Immunity --- p.14
Chapter 1.3 --- PHYTOCHEMICALS AS POTENTIAL IMMUNOMODULATORS and anti-tumour agents --- p.15
Chapter 1.3.1 --- Modulation of the Immune System --- p.15
Chapter 1.3.2 --- Induction of Cancer Cell Differentiation --- p.16
Chapter 1.3.3 --- Stimulation of Apoptosis --- p.17
Chapter 1.3.4 --- Other Anti-tumour Mechanisms --- p.18
Chapter 1.4 --- GREEN TEA: GENERAL PROPERTIES AND PHARMACO- logical activities --- p.19
Chapter 1.4.1 --- General Introduction --- p.19
Chapter 1.4.2 --- Chemistry of Tea --- p.21
Chapter 1.4.3 --- Physiological and Pharmacological Effects of Green Tea Catechins --- p.26
Chapter 1.4.3.1 --- Anti-oxidative Activity --- p.26
Chapter 1.4.3.2 --- Anti-mutagenic Activity --- p.27
Chapter 1.4.3.3 --- Anti-carcinogenic Activity --- p.27
Chapter 1.4.3.4 --- Anti-inflammatory Activity --- p.32
Chapter 1.4.3.5 --- Hypocholesterolemic and Hypolipidemic Activities --- p.32
Chapter 1.4.3.6 --- Anti-microbial Activity --- p.33
Chapter 1.5 --- aims and scopes of this investigation --- p.34
Chapter CHAPTER 2: --- MATERIALS AND METHODS
Chapter 2.1 --- MATERIALS --- p.36
Chapter 2.1.1 --- Animals --- p.36
Chapter 2.1.2 --- Cell lines --- p.36
Chapter 2.1.3 --- Green Tea Catechins and Epicatechin Isomers --- p.38
Chapter 2.1.4 --- Recombinant Murine Interleukin-2 (rmIL-2) --- p.38
Chapter 2.1.5 --- Antibodies --- p.39
Chapter 2.1.6 --- "Buffers, Culture Medium and Other Reagents" --- p.40
Chapter 2.1.7 --- Reagents for Gel Electrophoresis --- p.47
Chapter 2.1.8 --- Radioisotopes --- p.48
Chapter 2.2 --- METHODS --- p.49
Chapter 2.2.1 --- "Isolation, Purification and Characterization of Green Tea Catechins and Epicatechin Isomers" --- p.49
Chapter 2.2.1.1 --- Extraction of Green Tea Catechins --- p.49
Chapter 2.2.1.2 --- Analysis of Epicatechin Isomers by HPLC --- p.49
Chapter 2.2.1.3 --- Determination of the Bio-toxicity of Green Tea Catechins --- p.50
Chapter 2.2.1.4 --- Assay of In Vitro Cytotoxicity of Green Tea Catechins on Splenocytes --- p.51
Chapter 2.2.2 --- Assays for the Immunomodulatory Activities of Green Tea Catechins --- p.52
Chapter 2.2.2.1 --- Isolation and Preparation of Cells --- p.52
Chapter 2.2.2.2 --- In Vitro Lymphocyte Transformation Assay --- p.53
Chapter 2.2.2.3 --- Mixed Lymphocyte Culture --- p.53
Chapter 2.2.2.4 --- Colorimetric Assay of Alloreactive Cytotoxic T Lymphocytes --- p.54
Chapter 2.2.2.5 --- Foodpad Swelling Assay of Delayed-type Hypersensitivity --- p.55
Chapter 2.2.2.6 --- Haemagglutination Assay of In Vivo Antibody Formation --- p.56
Chapter 2.2.2.7 --- Characterization of the Lymphocyte Subpopulations from Spleen by Flow Cytometry --- p.56
Chapter 2.2.2.8 --- In Vivo Migration of Macrophages --- p.57
Chapter 2.2.2.9 --- In Vitro Assay of Phagocytic Activity of PEC --- p.58
Chapter 2.2.2.10 --- In Vitro Assay of Macrophage-mediated Cytostatic Activity --- p.58
Chapter 2.2.3 --- Assays for the Anti-tumour Activities of Green Tea Catechins --- p.60
Chapter 2.2.3.1 --- Assay of In Vivo Anti-tumour Activity --- p.60
Chapter 2.2.3.2 --- Induction and Assay of Natural Killer Cell Activity --- p.60
Chapter 2.2.3.3 --- Induction and Assay of Lymphokine-activated Killer Cell Activity --- p.61
Chapter 2.2.3.4 --- Assay of In Vitro Tumour Cell Proliferation --- p.62
Chapter 2.2.3.5 --- In Vitro Tumour Clonogenicity Assay --- p.63
Chapter 2.2.3.6 --- Induction of Myeloid Leukemic Cell Differentiation --- p.63
Chapter 2.2.3.7 --- DNA Fragmentation Analysis --- p.64
Chapter 2.2.3.8 --- Cell Cycle and DNA Content Evaluation --- p.66
Chapter 2.2.4 --- Statistical Analysis --- p.66
Chapter CHAPTER 3: --- "Extraction, Purification and Characterization of GTCs"
Chapter 3.1 --- INTRODUCTION --- p.67
Chapter 3.2 --- RESULTS --- p.69
Chapter 3.2.1 --- "Extraction of Catechins from the Chinese Green Tea, Ji Pin Long Jing" --- p.69
Chapter 3.2.2 --- Analysis of Epicatechin Isomers by HPLC --- p.69
Chapter 3.2.3 --- Bio-toxicity Determination by Brine Shrimp Bioassay --- p.71
Chapter 3.2.4 --- Effect of GTCs on the Viability of Murine Splenocytes --- p.72
Chapter 3.3 --- DISCUSSION --- p.74
Chapter CHAPTER 4: --- The Immunomodulatory Activities of GTCs
Chapter 4.1 --- INTRODUCTION --- p.75
Chapter 4.2 --- RESULTS --- p.77
Chapter 4.2.1 --- Effects of GTCs on the In Vitro Proliferation of Murine Splenocytes --- p.77
Chapter 4.2.2 --- In Vitro Co-mitogenic Effect of GTCs on Murine Splenocytes --- p.77
Chapter 4.2.3 --- Stimulation of Lymphocyte Proliferation In Vitro by Intraperitoneal Administration of GTCs --- p.81
Chapter 4.2.4 --- Effect of In Vivo Treatment of GTCs on In Vitro Mixed Lymphocyte Reaction --- p.81
Chapter 4.2.5 --- Effect of In Vivo Administration of GTCs on Splenic Lymphocytes Subpopulations --- p.87
Chapter 4.2.6 --- Effect of In Vivo Administration of GTCs on the Induction of Alloreactive Cytotoxic T Lymphocytes --- p.87
Chapter 4.2.7 --- In Vivo Induction of Delayed-type Hypersensitivity (DTH) Response to Sheep Red Blood Cells (SRBC) by GTCs --- p.91
Chapter 4.2.8 --- Primary Humoral Immune Response to SRBC in GTCs- treated Mice --- p.91
Chapter 4.2.9 --- Effect of GTCs on In Vivo Migration of Macrophages --- p.95
Chapter 4.2.10 --- Effect of GTCs on the Phagocytic Activity of Thioglycollate- elicited Macrophages In Vitro --- p.95
Chapter 4.2.11 --- Effect of In Vivo Administration of GTCs on Phagocytic Activity of Thioglycollate-elicited Macrophages In Vitro --- p.98
Chapter 4.2.12 --- Effect of GTCs on In Vitro Cytostatic Activity of Picolinic Acid-activated Macrophages --- p.98
Chapter 4.2.13 --- Effect of In Vivo Administration of GTCs on the Cytostatic Activity of Picolinic Acid-activated Macrophages --- p.101
Chapter 4.3 --- DISCUSSION --- p.103
Chapter CHAPTER 5: --- THE ANTI-TUMOUR ACTIVITIES OF GTCs
Chapter 5.1 --- introduction --- p.107
Chapter 5.2 --- RESULTS --- p.109
Chapter 5.2.1 --- Effects of GTCs on the Growth of Transplantable Tumour Cells In Vivo --- p.109
Chapter 5.2.2 --- Effect of GTCs on In Vivo Induction of Natural Killer Cells --- p.109
Chapter 5.2.3 --- Effect of GTCs on In Vitro Induction of Lymphokine- activated Killer Cell Activity --- p.113
Chapter 5.2.4 --- In Vitro Cytotoxicity of Green Tea Epicatechin Isomers on Murine and Human Tumour Cell Lines --- p.115
Chapter 5.2.5 --- In Vitro Cytostatic Effect of EGCG on Various Tumour Cell Lines --- p.118
Chapter 5.2.6 --- Effect of EGCG on the In Vitro Clonogenicity of Myeloid Leukemia Cells --- p.127
Chapter 5.2.7 --- Induction of Apoptosis of Myeloid Leukemia HL-60 Cells In Vitro --- p.130
Chapter 5.2.8 --- Effect of EGCG on the Cell Cycle Kinetics of Myeloid Leukemia HL-60 Cells In Vitro --- p.131
Chapter 5.2.9 --- Effect of EGCG on the Morphological Changes of Myeloid Leukemia Cells --- p.136
Chapter 5.2.10 --- Effect of EGCG on the Endocytic Activity of Myeloid Leukemia Cells --- p.136
Chapter 5.3 --- discussion --- p.141
Chapter CHAPTER 6: --- CONCLUSIONS AND FUTURE PERSPEC- TIVES --- p.145
REFERENCES --- p.152