Dissertations / Theses on the topic 'Neuroprotective agents'
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Nilsson, Olov. "Cannabinoids as neuroprotective agents : a mechanistic study." Doctoral thesis, Umeå : Umeå universitet, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-873.
Full textBadenhorst, Hester Elizabeth. "Antihistamines as neuroprotective agents / Hester Elizabeth Badenhorst." Thesis, North-West University, 2004. http://hdl.handle.net/10394/95.
Full textThesis (M.Sc. (Pharmaceutical Chemistry))--North-West University, Potchefstroom Campus, 2005.
Egunlusi, Ayodeji Olatunde. "Novel norbornane derivatives as potential neuroprotective agents." University of Western Cape, 2020. http://hdl.handle.net/11394/7339.
Full textNeurodegenerative disorders are characterised by progressive loss of the brain’s physiological functions as a result of gradual degeneration of neurons in the central nervous system. Even though they are classified as diseases of the elderly, occurrence earlier in life is possible, but that would suggest the influence of genetic and/or environmental factors. Due to the continuous rise in modernisation and industrialisation over the years, there has been an increase in incidence and prevalence of neurodegenerative disorders. With the advances in technology and life expectancy, the rates of the common forms (Alzheimer’s disease and Parkinson’s disease), are expected to increase exponentially by 2050. Unfortunately, there is still no clinically approved treatment or therapy to slow down or halt the degenerative process as most registered drugs only offer symptomatic relief. Confounding this issue is the lack of definite mechanism of neurodegeneration, which is still poorly defined and not completely understood. Nonetheless, the pathology of most neurodegenerative disorders is believed to be a combination of interrelated processes that eventually leads to neuronal cell death. Among the postulated processes, the impact of excitotoxicity mediated by NMDA receptor over-activation is prominent and it is implicated in virtually all neurodegenerative disorders. With this basic insight, it is believed that molecules capable of inhibiting NMDA receptors and associated calcium channels, without affecting the normal physiological functions of the brain, could potentially serve as good neuroprotective drugs. Competitive and uncompetitive blockers (MK-801 and ketamine) have been explored, but none were clinically accepted due to undesirable side effects such as hallucinations, sedation and depression. However, NGP1-01, a polycyclic cage molecule, has been shown to be neuroprotective through modulation of NMDA receptors and voltage gated calcium channels and attenuation of MPP+ -induced toxicity. A similar approach could be useful in the design and development of new neuroprotective drugs. The aim of this study was to synthesise a series of open and rearranged cage-like molecules and explore their neuroprotective potential in neuroblastoma SH-SY5Y cells. The proposed structures, with norbornane scaffolds that contained different moieties, were designed to structurally resemble NGP1-01 and MK-801. Once synthesised, the compounds were purified and characterised, and were evaluated for their biological activities. Compounds were first screened for cytotoxicity at different concentrations. Thereafter, they were evaluated for neuroprotective effects against MPP+ -induced excitotoxicity and for calcium flux modulatory effects on NMDA receptor and voltage gated calcium channels. The norbornane derivatives were synthesised and characterised, and all final products were afforded in sufficient yields. All compounds with the exception of two compounds displayed good cytotoxic profiles towards the SH-SY5Y neuroblastoma cells at 10 µM, 50 µM and 100 µM concentrations as they demonstrated percentage cell viabilities close to 100% (control treated cells). Only two compounds showed percentage cell viability of 51% and 59% at 100 µM. Utilising the same cell line, all compounds, tested at 10 µM, attenuated MPP+ -induced toxicity after 24 hours of exposure to a neurotoxin. This was evident in the 23% to 53% enhancement (significant with p < 0.05) in cell viability when compared to the MPP+ only treated cells. In comparison to known NMDA receptor and/or voltage gated calcium channel blockers (MK-801, NGP1-01 or nimodipine), the synthesised compounds demonstrated mono or dual inhibition of calcium channels as they effectively attenuated calcium influx by blocking NMDA receptors and/or voltage gated calcium channels expressed in neuroblastoma SHSY5Y cells. This group of compounds were found to be more potent NMDA receptor inhibitors, probably due to similarities with MK-801 and memantine, than voltage gated calcium channel inhibitors. All compounds demonstrated moderate to good calcium inhibitory effects at NMDA receptors in the range of 23% to 70% while a selected few displayed very little or no activity at the voltage gated calcium channels. In conclusion, 27 compounds with norbornane scaffolds were successfully synthesised and evaluated for cytotoxicity and neuroprotection. The abilities of the synthesised compounds to protect neurons from the neurotoxin MPP+ and reduce calcium flux into neuronal cells were successfully demonstrated. These characteristics are essential in neuroprotection as they may prove significant in halting or slowing down the disease progression. The compounds showing a good cytotoxicity profile, neuroprotective effects and ability to reduce calcium overload, could potentially act as neuroprotective agents with good safety profiles or contribute as lead structures to the development and design of structurally related molecules that could clinically benefit people with neurodegenerative disorders.
Kadernani, Yakub Esmail Y. E. "Novel adamantane derivatives as multifunctional neuroprotective agents." University of the Western Cape, 2013. http://hdl.handle.net/11394/4256.
Full textThe pathology of neurodegenerative disorders involves multiple steps, and it is probably for this reason that targeting one particular step in a multi-step process has only yielded limited results. Nitric oxide (NO) is synthesised from L-Arginine by an enzyme known as nitric oxide synthase (NOS). Three isoforms of NOS exist, including endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). In the central nervous system (CNS), nNOS is involved in the synthesis of NO, which is involved in various neurological functions. NO is a free radical and this probably explains why an excess amount of it has been implicated in the development of neurodegenerative disorders. In the CNS, the Nmethyl- D-aspartate (NMDA) receptor in its active state allows the influx of calcium ions which activate nNOS thus increasing the amount of NO and other detrimental reactive nitrogen species within neuronal cells. Calcium entry through voltage-gated calcium channels (VGCC) may also contribute to this. Although calcium ions are important for physiological functioning, an excess is responsible for excitotoxicity, which can ultimately lead to neurodegeneration. Our aim was to synthesise a series of adamantane-derived compounds that act at multiple target sites in the neurodegenerative pathway. By conjugating benzyl and phenylethyl moieties with different functional groups (-H, -NO2, -NH2, -NHC(NH)NH2, -OCH3) to the amantadine structure, we aimed to synthesise compounds that display calcium channel and NMDA receptor (NMDAR) channel inhibition, as well as selective inhibition of nNOS. A series of compounds (-H, -NO2, -NH2, -OCH3) were obtained in yields that varied between 16.5 % and 90.25 %. These novel compounds were tested for calcium influx through VGCC and NMDAR inhibition using synaptoneurosomes isolated from rat brain homogenate against the reference compounds MK-801, NGP1-01, amantadine, memantine and nimodipine. A lack of success with the synthesis of the guanidine compounds prevented the use of the oxyhemoglobin capture assay for the determination of nNOS inhibitory activity of these compounds. The novel synthesised compounds display inhibitory activity towards VGCC and the NMDAR in the micromolar range. Further tests are recommended on compounds SE-1, SE-4, SE-11 and SE-12 as they displayed good inhibitory activity against both NMDAR- as well as ii KCl-mediated calcium influx. These novel compounds may be better therapeutic options than amantadine and memantine as they inhibit both NMDAR and VGCC-mediated calcium influx, whereas amantadine and memantine only inhibit NMDA-mediated calcium influx. These novel adamantane derived compounds may possibly serve as novel leads or potential therapeutic agents for the treatment of neurodegenerative disorders.
Zindo, Frank T. "Polycyclic propargylamine derivatives as multifunctional neuroprotective agents." University of the Western Cape, 2018. http://hdl.handle.net/11394/6748.
Full textThe abnormal death of neurons in the central nervous system of individuals suffering from neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and amyotrophic lateral sclerosis, takes place by an intrinsic cell suicide programme known as apoptosis. This process is triggered by several stimuli, and consists of numerous pathways and cascades which lead to the death of neuronal cells. It is this multifactorial nature of neurodegenerative diseases that has over the years seen many researchers develop compounds that may serve as multi-target directed ligands (MTDLs) which could potentially confer neuroprotection by acting simultaneously on different receptors and target sites implicated in neurodegeneration. This study was aimed at developing MTDLs that may serve as neuroprotective agents by simultaneously (a) inhibiting N-methyl D-aspartate receptors (NMDAR) and blocking L-type voltage gated calcium channels (VGCC) thus regulating the Ca2+ influx mediated excitotoxic process; (b) inhibiting the monoamine oxidase enzymes A and -B (MAO-A/B) thus allowing increase in dopamine levels in the central nervous system and reducing the levels of the highly oxidative products produced by the activity of these enzymes; (c) possessing anti-apoptotic activity to halt the neuronal cell death process. In designing the compounds we focused on the structures of rasagiline and selegiline, two well-known MAO-B inhibitors and proposed neuroprotective agents, and of NGP1-01, a known VGCC blocker and NMDAR antagonist. The first series of compounds (reported in research article 1, Chapter 3), comprised polycyclic propargylamine and acetylene derivatives. Compounds 12, 15 and 16 from this series showed promising VGCC and NMDA receptor channel inhibitory activity ranging from 18 % to 59 % in micromolar concentrations, and compared favourably to the reference compounds. In the MAO-B assay, compound 10 exhibited weak MAO-B inhibition of 73.32 % at 300 μM. The rest of the series showed little to no activity on these target sites, despite showing significant anti-apoptotic activity. This suggested the compounds in this series to be exhibiting their neuroprotective action through some other mechanism(s) unexplored in this study.
Saathoff, John. "Curcumin/Melatonin Hybrids as Neuroprotective Agents for Alzheimer's disease." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4586.
Full textHobbs, Catherine E., and n/a. "Perinatal hypoxia-ischaemia : neuroprotective strategies." University of Otago. Department of Anatomy & Structural Biology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.145910.
Full textSinger, Cherie A. "Neurotrophic and neuroprotective effects of estrogen /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6301.
Full textMusakwa, Lovetone. "Chalcone and curcumin hybrids of indole propargylamines as multifunctional neuroprotective agents." University of the Western Cape, 2020. http://hdl.handle.net/11394/7959.
Full textNeurodegenerative disorders (NDs) are a range of chronic brain disorders that includes amongst others motor function loss. Parkinson’s disease (PD) is one of the common NDs that has an insidious onset and diagnosed when dopaminergic neurons in the substantia nigra are already lost. The loss creates a deficiency of the dopamine (neurotransmitter) thereby causing neurochemical imbalance resulting in the signs and symptoms of PD. NDs overlap at multiple levels so some of the symptoms overlap as well. NDs currently have no cure yet and current drug therapies only improve the quality of life of the patients by targeting the symptoms mainly. Treatment of PD currently involves different classes of drugs and depending on the stages of the disease, some drugs can be only used as an adjunct therapy. Anti-oxidants and monoamine oxidase inhibitors (MAO-I) are part of the treatment options.
Janis, Kelly Lynn. "Investigation of the efficacy of various neuroprotection agents for their potential use in the treatment of Parkinson's disease." Diss., Connect to online resource - MSU authorized users, 2008.
Find full textKaruppagounder, Senthilkumar S. Dhanasekaran Muralikrishnan Suppiramaniam Vishnu. "Environmental toxins and dopaminergic neurotoxicity novel neuroprotective strategies /." Auburn, Ala, 2009. http://hdl.handle.net/10415/1883.
Full textLi, Ka Wai. "Neuroprotective roles of cefriaxone on cultured astrocytes and neuronal cells." HKBU Institutional Repository, 2011. http://repository.hkbu.edu.hk/etd_ra/1277.
Full textLui, Nga Ping. "Endogenous neuroprotective mechanisms in early stages of rat parkinsonism." HKBU Institutional Repository, 2011. http://repository.hkbu.edu.hk/etd_ra/1251.
Full textSimi, Anastasia. "Molecular basis for the anti-inflammatory properties of chlomethiazole /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-621-9/.
Full textHo, Yuen-shan. "Investigation of lycium barbarum as neuroprotective drug against Alzheimer's disease." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43572388.
Full textWoo, Tak-yunn Tiffany, and 胡德欣. "Neuroprotective strategies in a rat model of retinal detachment." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48334911.
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Medicine
Master
Master of Research in Medicine
Nogueira, Carlos Renato Alves. "AvaliaÃÃo dos efeitos anticonvulsivantes e neuroprotetores da doxiciclina em ratos adultos jovens." Universidade Federal do CearÃ, 2008. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=2767.
Full textA Pilocarpina à um agonista colinÃrgico caracterÃstico por induzir convulsÃes que evoluem para status epilÃpticus, similar à epilepsia do lobo temporal humana. Neste presente trabalho, nÃs avaliamos a possÃvel aÃÃo neuroprotetora da doxiciclina, uma tetraciclina de segunda geraÃÃo, nas convulsÃes induzidas pela pilocarpina em ratos Wistar machos, que receberam pilocarpina (300mg/kg i.p) presenÃa ou na ausÃncia de doxiciclina (25 à 100 mg/kg) administrada intraperitonealmente uma vez ao dia durante sete dias. ApÃs a injeÃÃo de pilocarpina, foram observados os sinais colinÃrgicos perifÃricos, as latÃncias de 1 convulsÃo e de morte. Foram determinadas as concentraÃÃes de aminoÃcidos no cÃrtex temporal atravÃs de cromatografia lÃquida de alta eficiÃncia HPLC, e a atividade do sistema antioxidante, catalase e as dosagens dos nÃveis de TBARS e nitrito. Os resultados mostraram que a doxiciclina nÃo alterou os sinais colinÃrgicos perifÃricos, contudo aumentou a latÃncia decorrida para a primeira convulsÃo (1.6 a 5 vezes), quando comparada ao grupo (P300). Resultados semelhantes foram demonstrados com a latÃncia de morte, que foi aumentada de 1.9 a 9.9 vezes. Observou - se que o prÃ-tratamento com doxiciclina 50 mg/kg foi capaz de reduzir em 25% os nÃveis de MDA, 64% os nÃveis de nitrito e 67.7% a atividade da catalase no cÃrtex temporal desses animais, demonstrando com clareza seu potencial antioxidante. Interessantemente, a doxiciclina diminuiu as concentraÃÃes de glutamato de 28 a 33%, e aumentou GABA em 112 e 91%, nas dose de 50 e 100mg/kg respectivamente nos animais administrados com P300, Na maior dose, a droga alterou os nÃveis de aspartato e taurina, diminuindo em 61% aspartato enquanto elevou os nÃveis de taurina em cerca de 34%. Surpreendentemente, somente a menor dose alterou os nÃveis de glicina, aumentendo a concentraÃÃo deste aminoÃcido em 132%. Em conclusÃo, mostramos que o inÃcio e a intensidade das convulsÃes induzidas pela pilocarpina foram significativamente reduzidos pela doxiciclina. Portanto, pelo menos em parte, este mecanismo de aÃÃo parece estar relacionado a uma diminuiÃÃo nos nÃveis de aminoÃcidos excitatÃrios e a um aumento nas concentraÃÃes de aminoÃcidos inibitÃrios no cÃrtex temporal desses animais.
Pilocarpine is known to induce convulsions leading to status epilepticus, similar to the temporal lobe epilepsy in humans. In the present work, we evaluated the possible protection affored by doxycyvline, a 2nd generation tetracycline, agaist pilocarpine- induced convulsions in male Wistar rats (P300mg/kg, i.p) in the absence and in the presence of doxicycline (25 to 100 mg/kg i.p.) daily for 7 days.After the pilocarpine injection, all groups were observed for cholinergic signs, latency to the first convulsion and latency to death. Besides, amino acid concentrations in temporal cÃrtices were determined by RP-HPLC, as well catalase activity and levels of TBARS and Nitrite. Results showed that doxycycline did not alter cholinergic signs but increased the latency time to the first convulsion (1.6 to 5 times increase), as compared to P300, and the highest effect was observed with the dose of 25 mg/kg. Similar results were demonstrated to death latency that increased from 1.9 to 9.9 times with doxyciclyne at the doses of 25, 50 and 100 mg/kg. In fact we showed that the pre-treatment with doxycycline decreased in 25% MDA levels, 64% nitrite levels and 67.7% catalase activity. Interestingly, doxycycline decreased glutamate concentrations in 28 and 33% and increased GABA in 112 and 91% at the doses of 50 and 100mg/kg respectively. At the higher dose the drug altered aspartate and taurine concentrations, decreased aspartate levels in 61%, while increasing taurine levels in 34%. Surprisingly, only the lower dose altered glycine levels, increasing its concentration by 132%. In conclusion, we showed that the onset and intensity of pilocarpine-induced seizures were significantly reduced by doxycycline. Furthermore, at least in part, its mechanism of action seems to be mediated by the decrease and increase of excitatory and inhibitory aminoacids, respectively. In addiction the doxycycline capacity to reduce the oxidative stress associated with the pilocarpine-induced may also play a role
Rees, Daniel J. "Natural and synthetic GHSR1a agonists as neuroprotective agents in models of Parkinson's disease." Thesis, Swansea University, 2017. https://cronfa.swan.ac.uk/Record/cronfa40946.
Full textCESCON, ELEONORA. "Reversible and covalent protein kinase CK1δ inhibitors: potential neuroprotective agents in neurodegenerative diseases." Doctoral thesis, Università degli Studi di Trieste, 2023. https://hdl.handle.net/11368/3040842.
Full textBesides its well-known role in controlling the circadian rhythm and cancer, protein kinase CK1δ is involved in the onset of neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). This pleiotropic role of CK1δ makes it an attractive target for innovative therapeutic approaches. The aim of this PhD project is therefore to develop both CK1δ reversible and covalent inhibitors. The catalytic domain (aa. 1-296) of CK1δ was expressed and purified to obtain a pure, properly folded and enzymatically active recombinant protein for in vitro biochemical studies, to deeply characterize the kinase binding site and the interactions of our inhibitors, as well as to obtain co-crystal structures. As regards the development of ATP-competitive inhibitors, the [1,2,4]triazolo[1,5-a][1,3,5]triazine (TT) nucleus was investigated since it has already successfully demonstrated to mimic the ATP’s adenine ring in interacting with the kinase’s catalytic domain. Starting from a previous series of TT kinase inhibitors having diamine substituents at the 5 position, new triazolo-triazine 5,7-diamines were synthesized. In particular, a new sub-set of molecules in which the terminal amino group was substituted with different aromatic systems or less bulky groups to study the role of the steric hindrance in this position as any additional interactions with the catalytic pocket was designed. After chemical characterization, all the compounds were evaluated towards CK1δ through a luminescence based assay and the blood-brain barrier (BBB) permeability of the most active compounds was predicted using the PAMPA-BBB assay. Also, their cytotoxicity was investigated with the MTT assay. In parallel, covalent inhibitors of CK1δ were designed and synthesized by inserting different electrophilic moieties at the 2-position of the phenyl group of known CK1δ inhibitor scaffold. The catalytic lysine (Lys-38), was identified as the nucleophile target for the covalent bond formation. The synthesized compounds were tested on CK1δ and IC50 data revealed that the aldehyde moiety is the most suitable electrophile (IC50 = 241 nM). Several experiments were conducted to demonstrate the covalent inhibitory mechanism. Results of the assays performed to demonstrate the dependence of the inhibitory activity on time and ATP concentration suggest a mixed ATP-competitive/un-competitive behavior. TSA experiments confirmed the stabilizing effect of the ligand towards CK1δ. Furthermore, the covalent adduct formation was investigated through intact mass spectrometry experiments and first co-crystallization attempts were carried out. 1H-NMR studies allowed to assess the reactivity of the electrophilic warhead towards a lysine’s amino group surrogate. Notably, despite the presence of a polar aldehyde substituent, the covalent compound demonstrated to be able to passively permeate the BBB and the MTT assay resulted in a good cell viability showing also a potential neuroprotective action of the covalent derivative.
Ho, Yuen-shan, and 何宛珊. "Investigation of lycium barbarum as neuroprotective drug against Alzheimer's disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43572388.
Full textFernandes, Mara Yone Soares Dias. "Efeito neuroprotetor do α-bisabolol em camundongos submetidos à isquemia cerebral focal permanente." Universidade Federal do CearÃ, 2015. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=14886.
Full textO acidente vascular cerebral (AVE) à uma das principais causa de mortalidade no Brasil, acometendo cerca de 200.000 indivÃduos anualmente. A fisiopatologia do AVE isquÃmico envolve uma complexa cascata de eventos como a inflamaÃÃo e o estresse oxidativo que podem à morte neuronal e dÃficits cognitivos. O α-bisabolol à um Ãlcool sesquiterpeno, monocÃclico, que ocorre na natureza e à encontrado como constituinte majoritÃrio do Ãleo essencial sintÃtico da Matricaria chamomilla, que possui atividade antiinflamatÃria, antioxidante e anti-apoptÃtica jà descritas. Para avaliar o efeito neuroprotetor deste composto em camundongos submetidos à oclusÃo permanente da artÃria cerebral media (pMCAO), os animais foram prà e pÃs tratados com α-bisabolol nas doses de 50, 100 e 200 mg/kg, v.o, durante 24, 48, 72, 96 ou 120 horas apÃs a isquemia. Os animais foram avaliados 24h apÃs a isquÃmia para verificar a Ãrea de lesÃo isquÃmica, avaliaÃÃo neurolÃgica e atividade da mieloperoxidase. 72 horas apÃs a pMCAO, os testes de atividade locomotora, memÃria de trabalho e memÃria aversiva recente foram realizados. 96 horas apÃs a pMCAO foi realizado o teste do reconhecimento de objecto, e os animais foram eutanasiados para a realizaÃÃo da Imunohistoquimica para TNF-α, iNOS e GFAP e anÃlise histologica para Cresil violeta e Fluoro Jade C. Finalmente, 120h apÃs a isquemia, avaliou-se a memÃria espacial. O α-bisabolol reduziu significativamente a lesÃo isquemica e o dÃficit neurolÃgico e normalizou a atividade locomotora. O α-bisabolol mostrou proteÃÃo contra os dÃficits nas memÃrias de trabalho, espacial, reconhecimento de objeto e aversiva. O α-bisabolol (200 mg/kg) preveniu significativamente o aumento da MPO e TNF-α no cÃrtex temporal e o aumento do iNOS tanto no cÃrtex temporal como no estriado. Tambem preveniu o aumento da astrogliose nessas Ãreas. O α-bisabolol (200 mg/kg) mostrou protecÃÃo contra a morte neuronal. Os resultados do presente estudo mostraram que o α-bisabolol possui atividade neuroprotetora provavelmente devido a sua aÃÃo antiinflamatÃria, mas outros mecanismos nÃo podem ser descartados.
Stroke is the leading cause of mortality in Brazil, affecting about 200,000 individuals annually. The pathophysiology of ischemic stroke involves a complex cascade of events such as inflammation and oxidative stress which will lead to neuronal death and cognitive deficits. The α-bisabolol is a sesquiterpene alcohol, natural, monocyclic, found as main constituents of the essential oil of Matricaria chamomilla, which has anti-inflammatory, antioxidant and anti-apoptotic already described. To evaluate the neuroprotective effects of this compound in mice underwent permanent occlusion of the middle cerebral artery (pMCAO), the animals were pre and post treated with α-bisabolol at doses of 50, 100 and 200 mg / kg, orally for 24, 48, 72, 96 or 120 hours after pMCAO. The animals were evaluated 24 hours after ischemia to verify the area of ischemic damage, and neurological evaluation and myeloperoxidase activity. Seventy-two hours after pMCAO, the locomotor activity tests, working memory and aversive recent memory were performed. Ninety six hours after the pMCAO was performed the object recognition test, and the animals were euthanized for carrying out the immunohistochemistry for TNF-α, iNOS and GFAP and for histology analyes Cresil violet and Fluoro Jade C. Finally, 120 h after pMCAO, the spatial memory was evaluated. The α-bisabolol reduced significantly ischemic damage and neurological deficit and normalized the locomotor activity. The α-bisabolol showed protection against the deficits in working, spatial, object recognition and aversive memories. The α-bisabolol (200 mg / kg) significantly prevented the increase of MPO and TNF-α in the temporal cortex and the increased of iNOS both in the temporal cortex and in striatum. Also prevented the increase in astrogliosis in there area. The α-bisabolol (200 mg / kg) showed protection against neuronal death. The results of this study showed that α-bisabolol has neuroprotective activity probably due to its anti-inflammatory action, but other mechanisms can not be discarded.
Rogers, Derek Charles. "The effects of neuroprotective agents on in vitro and in vivo models of neurotoxicity." Thesis, University of Hertfordshire, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283890.
Full textRamsunder, Adrusha. "An investigation into the possible neuroprotective or neurotoxic properties of metrifonate." Thesis, Rhodes University, 2005. http://hdl.handle.net/10962/d1007560.
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Rizzi, Caterina. "NGF steers microglia toward a neuroprotective phenotype." Doctoral thesis, Scuola Normale Superiore, 2019. http://hdl.handle.net/11384/85996.
Full textLi, Hongying, and 李洪英. "Secondary degeneration after partial optic nerve transection : mechanisms and the neuroprotective effects of lycium barbarum." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/197129.
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Anatomy
Doctoral
Doctor of Philosophy
Bienemann, Alison Sarah. "Assessing viral vectors as gene therapy agents and the study of neuroprotective effects of HSP70." Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492644.
Full textElabi, Osama. "The effect of L-dopa and neuroprotective agents on cell replacement therapy for Parkinson's disease." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/103900/.
Full textLau, Yuk-fan Silvania, and 劉玉芬. "The neuroprotective effect of lycium barbarum polysaccharides on retinal neurons in a novel acute glaucoma attack animal model." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47309325.
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Anatomy
Master
Master of Philosophy
Xiu, Jin. "Distribution and function of nicotinic acetylcholine receptors in glia cells and neurons with focus on the neuroprotective mechanisms of cholesterol-lowering drugs in Alzheimer's disease /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-758-8/.
Full textPalvie, Stefanie Michelle. "An investigation into the neuroprotective effects of dehydroepiandrosterone." Thesis, Rhodes University, 2006. http://hdl.handle.net/10962/d1003260.
Full textWong, Kai-hei Harmony, and 黃啟希. "Neuroprotective effects of lycium barbarum polysaccharide on corticosterone-induced damage on retinal ganglion cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48395110.
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Anatomy
Master
Master of Medical Sciences
Syers, Jacqueline Ann. "An evaluation of potential neuroprotective strategies in rats with partial MPP+ or 6-OHDA lesions of the substantia nigra." Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.265250.
Full textYang, Di, and 楊荻. "Neuroprotective effects of lycium barbarum extracts in cerebral and retinal ischemia/reperfusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206738.
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Ophthalmology
Doctoral
Doctor of Philosophy
Page, Cecilia. "Histone deacetylase inhibitors as novel neuroprotective agents in in vitro and in vivo models of Parkinson's disease." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/histone-deacetylase-inhibitors-as-novel-neuroprotective-agents-in-in-vitro-and-in-vivo-models-of-parkinsons-disease(ad783896-81f9-46db-a81f-3cf7b4d372fc).html.
Full textDairam, Amichand. "An investigation into the neuroprotective properties of the non-steroidal anti-inflammatory agents tolmetin, sulindac and turmeric." Thesis, Rhodes University, 2006. http://hdl.handle.net/10962/d1003230.
Full textZheve, Georgina Teurai. "Neuroprotective mechanisms of nevirapine and efavirenz in a model of neurodegeneration." Thesis, Rhodes University, 2008. http://hdl.handle.net/10962/d1003285.
Full textClarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.
Full textSong, Juxian, and 宋聚先. "Protective effects of chrysotoxine on Parkinsonian neurotoxins induceddopaminergic neuronal cell death in SH-SY5Y cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47150129.
Full textScheepers, Mark Wesley. "An investigation into the neuroprotective and neurotoxic properties of levodopa, dopamine and selegiline." Thesis, Rhodes University, 2008. http://hdl.handle.net/10962/d1003267.
Full textWang, Ziying. "Neuroprotective effects of a novel TFEB activator E4 and its self-carried nanoparticles in MPTP-induced Parkinson's disease models." HKBU Institutional Repository, 2019. https://repository.hkbu.edu.hk/etd_oa/695.
Full textKamdem, Jean Paul. "Antioxidant and neuroprotective properties of trichilia catigua (catuaba) against ischemia-reperfusion and pro-oxidants agents in rat hippocampal slices." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/78130.
Full textMedicinal plants have been shown to have beneficial effects against oxidative stress-induced pathophysiology of various diseases including brain ischemia-reperfusion (I/R). Trichilia catigua, popularly known in Brazil as “catuaba”, is widely used as a neurostimulant and aphrodisiac. Infusions of the bark are popularly used in folk medicine against sexual weakness, exhaustion, insomnia, stress, memory and central nervous systems disabilities. However, the involvement of antioxidant ability of T. catigua in its pharmacological properties especially in the management of neurological-related diseases is scanty in the literature. In this context, the first part of this study investigated the potential antioxidant activity of T. catigua using chemical and biological models. As a result, we have demonstrated that ethanolic extract and different fractions from the stem bark of T. catigua scavenged the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical, and inhibited the formation of thiobarbituric acid reactive substances (TBARS) caused by Fe2+ in rat’s brain homogenates. However, ethanolic extract exhibited the highest antioxidant activity. In addition, ethanolic extract inhibited Ca2+-induced reactive oxygen/nitrogen species (ROS/RNS) generation and caused a decrease in the mitochondrial membrane potential (ΔΨm) only at high concentrations. On the basis of the aforementioned results, we hypothesized that ethanolic extract from T. catigua may at least, markedly reduce oxidative damage induced by in vitro I/R in rat hippocampal slices through attenuation of ROS/RNS production. Thus, the second part of this study investigated the protective effects of ethanolic extract of T. catigua against oxidative damage induced by I/R in rat hippocampal slices. T. catigua prevents hippocampal slices from the deleterious effects caused by I/R, by increasing mitochondrial viability, which was associated with decreased lactate dehydrogenase (LDH) leakage in the incubation medium; by decreasing DCFH oxidation in the medium, and increasing non-protein thiols (NPSH) content in slices homogenates. In contrast, T. catigua could not protect slices from I/R when it was added to the medium after ischemic insult, suggesting that it can only be used as preventive and not as curative agent against brain damage. Taking that alteration in learning and memory function are common consequences of a wide variety of toxic insults and disease states, the third part of this study was undertaken to determine whether T. catigua offered neuroprotection against oxidative stress induced by different pro-oxidants. Exposure of rat hippocampal slices for 1 h to hydrogen peroxide (H2O2), sodium nitroprusside (SNP) and 3-nitropropionic acid (3-NPA) decreased mitochondrial activity, increased ROS/RNS in the incubation medium and caused TBARS formation in rat hippocampal slices homogenates. These deleterious effects were significantly attenuated by pre-treatment of slices with ethanolic extract of T. catigua. Overall, our data showed that the use of T. catigua extract may be beneficial in preventing neurological disorders associated with oxidative stress, and that its beneficial effects seems to be related at least, in part, to its antioxidant activity, which can be attributed to its polyphenolic content.
Sutherland, Brad Alexander, and n/a. "Heme oxygenase and the use of tin protoporphyrin in hypoxia-ischaemia-induced brain damage : mechanisms of action." University of Otago. Department of Pharmacology & Toxicology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090119.150318.
Full textMi, Xuesong, and 米雪松. "Neurodegeneration and neuroprotection in glaucoma retinopathy-probing the role of endothelin-1, RAGE, A{221} and lycium barbarum." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47243922.
Full textpublished_or_final_version
Anatomy
Doctoral
Doctor of Philosophy
Sartori, César Renato 1973. "Atividade fisica e neuroproteção em camundongos adultos após indução de status epilepticus por pilocarpina." [s.n.], 2005. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314234.
Full textDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
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Resumo: O modelo de epilepsia induzida por pilocarpina em camundongos reproduz a Epilepsia do Lobo Temporal (ELT) em humanos. Animais submetidos à indução de status epilepticus apresentam alterações comportamentais, eletroencefalográficas e lesão neuronal compatíveis com esta condição. Estudos recentes relatam relevantes efeitos positivos da prática de atividade física sobre o sistema nervoso tanto em humanos como em modelos animais. Dentre estes efeitos figuram o aumento da sobrevivência neuronal e da resistência cerebral a diferentes insultos, promoção da angiogênese, estímulo da neurogênese, fortalecimento da potenciação de longa duração no hipocampo, melhora da aprendizagem e memória e contribuição para a manutenção da função cognitiva durante o envelhecimento. Todos estes efeitos conferem à atividade física um grande potencial neuroprotetor. Além disso, foram relatados benefícios decorrentes desta intervenção ambiental diretamente em pacientes com epilepsia e em animais submetidos à epilepsia induzida. Contudo, não há dados na literatura sobre o possível efeito neuroprotetor da atividade física no modelo de epilepsia induzida por pilocarpina em camundongos. Assim sendo, o presente estudo teve por objetivo investigar os efeitos da atividade física voluntária crônica sobre a perda neuronal no hipocampo e suas conseqüências na função mnemônica de camundongos submetidos a este modelo experimental. Trinta e dois camundongos Swiss foram divididos em quatro grupos experimentais (n=8): Saudável Sedentário (SS), Saudável Corredor (SC), Epiléptico Sedentário (ES) e Epiléptico Corredor (EC). Quarenta e oito horas após a indução do status epilepticus, ou sua simulação, foi proporcionado aos animais dos grupos corredores (SC e EC) o acesso a uma roda de atividade instalada em suas respectivas gaiolas por um período de 28 dias. Após este período os animais foram testados no labirinto aquático de Morris para avaliação da memória de referência espacial. Ao final dos testes os animais foram perfundidos com paraformaldeído (4% em tampão fosfato) e os cérebros removidos e processados para inclusão em parafina. Foram então obtidos cortes frontais do cérebro (8µm) para avaliação da extensão da lesão tecidual (coloração de Nissl), da presença de neurônios em degeneração (Fluoro Jade B) e da proliferação celular (PCNA) na formação hipocampal dorsal. Os animais dos grupos SS e SC não apresentaram lesão neuronal ou neurodegeneração, como esperado; também não diferiram entre si na proliferação celular e no teste de memória de um modo geral. Os animais dos grupos ES e EC apresentaram lesão neuronal e neurodegeneração, não sendo constatadas diferenças entre sedentários e corredores. Por outro lado, os animais ES revelaram maior proliferação celular comparados aos EC. Os animais do grupo EC apresentaram desempenho significativamente melhor nos testes de memória quando comparados aos animais ES. Assim, nossos dados revelaram que, a despeito de não ter ocorrido proteção contra lesão histológica, a atividade física melhorou significantemente o desempenho dos animais submetidos ao status epilepticus no teste do labirinto aquático de Morris, indicando que mesmo após lesão neurológica a atividade física promove melhora funcional. Acreditamos que tal melhora pode ser atribuída a mecanismos moleculares relacionados à plasticidade neuronal, que não foram identificados pelas técnicas utilizadas no presente estudo
Abstract: Pilocarpine-induced epilepsy in mice is an experimental model of the Temporal Lobe Epilepsy (TLE). Status epilepticus determined by pilocarpine adminstration leads to behavioral and electroencephalographic changes and neuronal damage similar to those observed in TLE. Recently, it has been shown that physical activity exerts neuroprotective effects, such as increase in neuronal survival, angiogenesis and neurogenesis; resistance to brain injuries, strengthening of the long term potentiation (LTP), improvement of memory and learning; and preservation of cognitive function during aging process. Particularly, physical activity also plays a positive role in epileptic patients and animals. However, there are no reports regarding the neuroprotective action of physical activity on the pilocarpine model of epilepsy in mice. In the present work, we studied the effects of the voluntary physical activity on hippocampal neuronal loss and mnemonic function of mice after the pilocarpine-induced status epilepticus. Thirty-two Swiss mice were assigned to four experimental groups (n=8): Normal Sedentary (NS), Normal Runner (NR), Epileptic Sedentary (ES) and Epileptic Runner (ER). Forty-eight hours after the status epilepticus or its simulation the animals of the runner groups (NR, ER) had access to a running wheel for 28 days. After that, the mice were submitted to the Morris Water Maze test for the evaluation of the spatial memory. Finally, the mice were perfused with paraformaldehyde (4% in phosphate buffer), the brains were dissected and processed for paraffin embedding. Frontal sections (8mm) were serially cut and used for analysis of histologic damage (Nissl staining), degenerating neurons (Fluoro Jade B) and cell proliferation (immunohistochemistry for PCNA) of the dorsal hippocampal formation. Mice of the NS and NR groups showed neither neuronal damage nor neurodegeneration. In addition, these groups were similar to each other in the Morris Water Maze test and exhibited comparable immunostainig patterns for PCNA. In contrast to the previous groups, in ES and ER groups neuronal damage and neurodegeneration were observed and equivalent. However, cell proliferation was higher in ES than in ER. Animals of the ER group had better performance in the Morris Water Maze test compared to ES mice. In conclusion, our results show that physical activity improved significantly the spatial memory of mice that had status epilepticus induced by pilocarpine, despite of having not changed the morphological evidence of neuronal damage. We believe that such improvement might be attributed to molecular mechanisms related to neuronal plasticity, which were not identified by the techniques we used in the present investigation
Mestrado
Fisiologia
Mestre em Biologia Funcional e Molecular
Lorente, Picon Marina. "Neuroprotective effect of stomatin-like protein 2 overexpression in A53T-a-synuclein parkinson disease mice model." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66338.
Full textKundrotienė, Jurgita. "Ischemic brain damage following transient and moderate compression of sensorimotor cortex in Sprague-Dawley and diabetic Goto-Kakizaki rats /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-819-X/.
Full textAvery, Michelle A. "Axon Death Prevented: Wlds and Other Neuroprotective Molecules: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/520.
Full textVázquez, Jiménez Laura. "Studies on the Chemical Modulation of Neuroprotective Agents Related to CR-6 Addressed to Improve the Delivery through the Blood-Brain Barrier." Doctoral thesis, Universitat de Barcelona, 2014. http://hdl.handle.net/10803/285339.
Full textEl estrés oxidativo es uno de los factores etiológicos más importantes en las enfermedades degenerativas como el cáncer, el Alzheimer o en episodios de isquemia. Durante estos procesos, se generan especies reactivas de oxigeno (ROS) y de nitrógeno (RNS) que provocan modificaciones de las biomoléculas como los lípidos, las proteínas y el ADN. El uso de agentes antioxidantes y neuroprotectores ayudan a reducir los efectos lesivos que el estrés oxidativo tiene en el cerebro, por ejemplo. La barrera hematoencefálica o BBB protege al cerebro de la acción de una amplia variedad de moléculas orgánicas y fármacos. Por ello, existe un gran interés en el desarrollo de nuevos agentes antioxidantes con un buen transporte a través de la BBB. En nuestro grupo de investigación se ha desarrollado el agente antioxidante 3,4-dihidro-2,2-dimetil-7-metoxi-1-(2H)-benzopirano (CR-6), un análogo de alfa- y gamma-tocoferol, que en la actualidad se emplea en dermofarmacia y se encuentra en ensayos de fase II para el tratamiento del cáncer (combinado con otros fármacos). En este proyecto se persigue la síntesis de una colección de análogos del CR-6 que mejoren el paso a través de la BBB. De este modo, se han sintetizado catorce compuestos derivados del CR-6 introduciendo nutrientes esenciales del cerebro que actúan como transbordadores de la BBB. La actividad antioxidante de todos estos compuestos se ha evaluado para asegurar que ésta se mantiene al introducir variabilidad en la posición C2 mediante los ensayos del DPPH y el in vitro CAA. A su vez, la permeabilidad de la BBB se ha evaluado para compararla con los compuestos de referencia CR-6 y Trolox a partir de los ensayos in vitro Caco-2, PAMPA y BBCEC.
Galpern, Wendy R. "Neuroprotection and Neurotransplantation Strategies in Models of Parkinson’s Disease." eScholarship@UMMS, 1996. https://escholarship.umassmed.edu/gsbs_diss/143.
Full textMacri, Fábio Teixeira. "Estudo do efeito neuroprotetor da estimulação magnética transcraniana e hipotermia em modelo de isquemia cerebral induzida." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/5/5166/tde-05092011-154945/.
Full textIntroduction: Over the time many researches have been conducted with the aim of identifying agents that may have beneficial effects in the treatment or prevention of cerebral ischemia, hypothermia has shown consistent results in experimental trials and Repetitive Trans Cranial Magnetic Stimulation (rTMS) has been used in a study attempting to reduce damage in hippocampal neurons. With the property to increase or decrease cortical excitability from the repetitive magnetic stimulus, it is estimated that an interference occurs in the production of some neurotransmitters and receptors of neuronal membrane, which therefore protects these cells from hypoxia. In this study we evaluated the ability of rTMS to protect neurons from injury due to hypoxia, and its possible interference in the protective effect of hypothermia and we tried to identify some mechanisms that possibly are involved in this phenomenon. Methods: Ischemia model was performed using Gerbil that was subsequently submitted to an evaluation of behavior and memory through passive avoidance task. The rTMS protocol was daily sessions with 25 series of 5 seconds at 25Hz with an interval of 45 seconds between series, for 7 consecutive days, with a total of 21 875 pulses with an intensity of 100% of motor threshold, and being carried through the induction of ischemia soon after the end of the last session, or rTMS after ischemia, in daily sessions with 25 series of 5 seconds at 25Hz with an interval of 45 seconds between series, for 3 consecutive days, starting immediately after surgery. The temperature of 36 °C was maintained during the period of vessel occlusion and subsequent 30 minutes, or 31 °C to 32 °C when in hypothermia. The preparation of the slices had sections of the region involving the hippocampus, stained with hematoxylin and eosin in addition to other preparations, TUNEL and caspase, which aim to evidence the occurrence of apoptosis. Results: Although not statistically significant, animals that received rTMS, apparently had better performance in passive avoidance task especially when applied after ischemia. The hypothermia demonstrated a significant efficiency, both in the histological analysis and in the passive avoidance task, associated or not to applications of rTMS and, in these animals undergoing ischemia during hypothermia, the ones who received rTMS had survival area in hippocampus significantly higher in histological analysis with hematoxylin and eosin. In animals undergone to ischemia during normal temperature, the rTMS has not shown to increase the area of hippocampal cell survival. Conclusions: rTMS (placebo or active, after or before the ischemia) seems to have a positive effect on passive avoidance task. The stimulation procedure appeared to be very traumatic and stressful for the animal, in which a few deaths occurred during the procedure, probably from asphyxiation due to restraint. The rTMS had a significant protective effect only in animals undergoing ischemia during hypothermia, as demonstrated in the histological analysis with hematoxylin and eosin