Gotowa bibliografia na temat „Glycation inhibitors”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Glycation inhibitors”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Glycation inhibitors"
1
Perera, HKI, i DCR Wijetunge. "A novel in vitro method to detect inhibitors of protein glycation". Asian Journal of Medical Sciences 5, nr 3 (24.02.2014): 15–21. http://dx.doi.org/10.3126/ajms.v5i3.8670.
Pełny tekst źródłaStreszczenie:
Background: Protein glycation generates advanced glycation end products (AGEs) which are implicated in the pathogenesis of chronic complications associated with diabetes. Identifi cation of medicinal plants with protein glycation inhibitory potential will enhance the opportunity to delay or inhibit diabetic complications with minimum side effects. Techniques available to identify protein glycation inhibitors require expensive specialized equipment. Objective: Objective of this study was to develop a relatively simple in vitro method to identify the protein glycation inhibitory potential of compounds or medicinal plants. Methods: Bovine serum albumin (BSA) was incubated with different concentrations of glucose or fructose or ribose for 31 days at pH 7.4. Standard inhibitor aminoguanidine (AG) was used as a positive control. Effect on the BSA migration under different experimental conditions was compared using polyacrylamide gel electrophoresis under native conditions (PAGE). Murraya koenigii leaf extract was analyzed for its effect on protein glycation. Results: We demonstrated many aspects of protein glycation including the effect of sugar concentration, type of the sugar and incubation period on protein glycation using this comparatively simpler method, which was previously, demonstrated using more sophisticated and expensive equipment. Migration of the BSA band towards the anode was proportionate to the degree of protein glycation. Further, we were innovative in demonstrating the inhibitory effect of AG on protein glycation using PAGE. BSA migration was comparatively slower when AG was included in the presence of sugar, indicating its inhibitory effects. We also revealed the protein glycation inhibitory potential of Murraya koenigii leaf extract, which was greater than that of AG at the concentrations used in the study. Conclusion: We have developed novel simple in vitro method using PAGE to identify inhibitors of protein glycation. Asian Journal of Medical Science, Volume-5(3) 2014: 15-21 http://dx.doi.org/10.3126/ajms.v5i3.8670
2
E-FARAN, MISS GULL, MUHAMMAD ANJUM ZIA i NIGHAT ASLAM. "EFFECT OF CAPTOPRIL". Professional Medical Journal 19, nr 01 (3.01.2012): 078–85. http://dx.doi.org/10.29309/tpmj/2012.19.01.1929.
Pełny tekst źródłaStreszczenie:
Objectives: (1) To investigate the inhibitory effect of Captopril on level of glycation (in vivo). (2) To study glycation inhibition invivo. Study design: Case study. Period: Sep. 2006 to March. 2008. One year seven months. Setting: Department of Biochemistry Universityof Agriculture, Faisalabad. Methods: Different parameters like fluorescence, total proteins, TBA (thiobarbituric acid) method, periodateborohydride assay were used to check the effect of inhibitor on glycation. Thirty two combinations were made and all these combinations wereplaced at 37̊C, at same time for five weeks. 3mL of blood sample was drawn after 1st, 3rd and 5th week of incubation to perform the experimentsfor glycation and glycation inhibition. Along with the same temperature (37̊C), different combinations of glucose and inhibitor were used.Results: Effective concentration of inhibitor helped to decrease the level of glycation. All concentrations of glucose (G , G and G ) showed 1 2 3glycation with protein. The inhibitor Captopril (all concentrations) showed variations in inhibition of glycation at one temperature (37̊C) withdifferent parameters (Fluorescence, TBA and Periodate) but the most effective concentration of inhibitors at each condition is I (1mM) but I (10 3 1mM) and I (5 mM) were also equally effective after I . Periodate borohydride Assay is more effective for glycation determination than 2 3thiobarbituric acid assay. Conclusions: Captopril can be used as glycation inhibitor in future. As it enhances the activity of transketolase, it canproduce 3DG compound which can block the AGEs. However, more experimentations should be done on animal or on large scale before itsapplication in diabetic patients.
3
Pawlukianiec, Cezary, Małgorzata Ewa Gryciuk, Kacper Maksymilian Mil, Małgorzata Żendzian-Piotrowska, Anna Zalewska i Mateusz Maciejczyk. "A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies". Pharmaceuticals 13, nr 9 (10.09.2020): 240. http://dx.doi.org/10.3390/ph13090240.
Pełny tekst źródłaStreszczenie:
Meloxicam is a non-steroidal anti-inflammatory drug, which has a preferential inhibitory effect to cyclooxyganase-2 (COX-2). Although the drug inhibits prostaglandin synthesis, the exact mechanism of meloxicam is still unknown. This is the first study to assess the effect of meloxicam on protein glyco-oxidation as well as antioxidant activity. For this purpose, we used an in vitro model of oxidized bovine serum albumin (BSA). Glucose, fructose, ribose, glyoxal and methylglyoxal were used as glycating agents, while chloramine T was used as an oxidant. We evaluated the antioxidant properties of albumin (2,2-di-phenyl-1-picrylhydrazyl radical scavenging capacity, total antioxidant capacity and ferric reducing antioxidant power), the intensity of protein glycation (Amadori products, advanced glycation end products) and glyco-oxidation (dityrosine, kynurenine, N-formylkynurenine, tryptophan and amyloid-β) as well as the content of protein oxidation products (advanced oxidation protein products, carbonyl groups and thiol groups). We have demonstrated that meloxicam enhances the antioxidant properties of albumin and prevents the protein oxidation and glycation under the influence of various factors such as sugars, aldehydes and oxidants. Importantly, the antioxidant and anti-glycating activity is similar to that of routinely used antioxidants such as captopril, Trolox, reduced glutathione and lipoic acid as well as protein glycation inhibitors (aminoguanidine). Pleiotropic action of meloxicam may increase the effectiveness of anti-inflammatory treatment in diseases with oxidative stress etiology.
4
West, Brett J., Shixin Deng, Akemi Uwaya, Fumiyuki Isami, Yumi Abe, Sho-ichi Yamagishi i C. Jarakae Jensen. "Iridoids are natural glycation inhibitors". Glycoconjugate Journal 33, nr 4 (15.06.2016): 671–81. http://dx.doi.org/10.1007/s10719-016-9695-x.
Pełny tekst źródła
5
Hosseini, Asieh, i Mohammad Abdollahi. "Diabetic Neuropathy and Oxidative Stress: Therapeutic Perspectives". Oxidative Medicine and Cellular Longevity 2013 (2013): 1–15. http://dx.doi.org/10.1155/2013/168039.
Pełny tekst źródłaStreszczenie:
Diabetic neuropathy (DN) is a widespread disabling disorder comprising peripheral nerves' damage. DN develops on a background of hyperglycemia and an entangled metabolic imbalance, mainly oxidative stress. The majority of related pathways like polyol, advanced glycation end products, poly-ADP-ribose polymerase, hexosamine, and protein kinase c all originated from initial oxidative stress. To date, no absolute cure for DN has been defined; although some drugs are conventionally used, much more can be found if all pathophysiological links with oxidative stress would be taken into account. In this paper, although current therapies for DN have been reviewed, we have mainly focused on the links between DN and oxidative stress and therapies on the horizon, such as inhibitors of protein kinase C, aldose reductase, and advanced glycation. With reference to oxidative stress and the related pathways, the following new drugs are under study such as taurine, acetyl-L-carnitine, alpha lipoic acid, protein kinase C inhibitor (ruboxistaurin), aldose reductase inhibitors (fidarestat, epalrestat, ranirestat), advanced glycation end product inhibitors (benfotiamine, aspirin, aminoguanidine), the hexosamine pathway inhibitor (benfotiamine), inhibitor of poly ADP-ribose polymerase (nicotinamide), and angiotensin-converting enzyme inhibitor (trandolapril). The development of modern drugs to treat DN is a real challenge and needs intensive long-term comparative trials.
6
Julius, Angeline, i Waheeta Hopper. "INHIBITION OF ADVANCED GLYCATION END-PRODUCT FORMATION BY QUERCETIN AND CATECHIN: AN ALTERNATIVE THERAPY FOR TREATING DIABETIC COMPLICATIONS". Asian Journal of Pharmaceutical and Clinical Research 10, nr 11 (1.11.2017): 173. http://dx.doi.org/10.22159/ajpcr.2017.v10i11.19412.
Pełny tekst źródłaStreszczenie:
Objective: The objective of this research was to determine early advanced glycation end-product (AGE) inhibition by natural aldose reductase inhibitors (ARIs), quercetin and catechin.Methods: The assay mixture (4 ml) consisted of 2 ml of 50 mM phosphate-buffered saline (pH 7.4), 50 μg/μl bovine serum albumin (BSA), and 2 mM glucose with or without the inhibitor. The test samples were treated with three different concentrations (10 mM, 20 mM, and 40 mM) of quercetin and catechin. High-throughput screening-based assay was adapted to perform the BSA-glucose test to determine the induction of AGE formation and its inhibition by quercetin, and catechin, using the fluorescence of the AGE-BSA sample at excitation and emission wavelengths of 350 and 450 nm.Result: The ARIs, quercetin and catechin inhibited early glycation with an inhibitory concentration value of 15.58 mM and 35.01 mM, respectively.Conclusion: The suppression of AGEs formation by natural inhibitors of aldose reductase would provide an alternative approach to the control of diabetic complications.
7
Pervez, Humayun, Nazia Khan, Jamshed Iqbal, Sumera Zaib, Muhammad Yaqub, Muhammad Nawaz Tahir i Muhammad Moazzam Naseer. "Synthesis, crystal structure, molecular docking studies and bio-evaluation of some N4-benzyl-substituted isatin- 3-thiosemicarbazones as urease and glycation inhibitors". Heterocyclic Communications 24, nr 1 (23.02.2018): 51–58. http://dx.doi.org/10.1515/hc-2017-0148.
Pełny tekst źródłaStreszczenie:
Abstract Fifteen N4-benzyl-substituted isatin-3-thiosemicarbazones 5a–o were synthesized and evaluated for their urease and glycation inhibitory potential. Lemna aequinocitalis growth and Artemia salina assays were also done to determine their phytotoxic and toxic effects. All compounds are potent inhibitors of the urease enzyme, displaying inhibition [half maximal inhibitory concentration (IC50)=1.08±0.12–11.23±0.19 μm] superior to that of the reference inhibitor thiourea (IC50=22.3±1.12 μm). Compounds 5c, 5d, 5h, 5j,k are potent antiglycating agents, showing glycation inhibitory activity better than that of the reference inhibitor rutin (IC50 values 209.87±0.37–231.70±6.71 vs. 294.5±1.5 μm). In the phytotoxicity assay, 11 thiosemicarbazones 5a–d, 5g, 5h, 5j–l, 5n,o are active, demonstrating 5–100% growth inhibition of L. aequinocitalis at the highest tested concentrations (1000 or 500 μg/mL). In the brine shrimp (A. salina) lethality bioassay, three derivatives 5b, 5j and 5o are active with median lethal dose (LD50) values of 3.63×10−5, 2.90×10−5 and 2.31×10−4 m, respectively.
8
Starowicz, Małgorzata, i Henryk Zieliński. "Inhibition of Advanced Glycation End-Product Formation by High Antioxidant-Leveled Spices Commonly Used in European Cuisine". Antioxidants 8, nr 4 (15.04.2019): 100. http://dx.doi.org/10.3390/antiox8040100.
Pełny tekst źródłaStreszczenie:
Spices and herbs, as good sources of polyphenols, could be strong inhibitors of advanced glycation end-product (AGE) formation. The aim of this research was to measure the ability of various spices to inhibit AGEs and to study the correlation of AGE inhibition with total phenolic (TP) content and antioxidant capacity. Fourteen spices commonly used in European cuisine were extracted with a 50% ethanol solution, and their water and total phenolic contents and antioxidant capacities were examined. Antioxidant capacity was evaluated using three methods: (1) Measurement of the radical scavenging ability of 2,2’-azino-bis-(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) and (2) 2,2-diphenyl-1-picrylhydrazyl (DPPH●); and (3) photochemiluminescence (PCL) assay. Antiglycation properties were studied in vivo using two model systems: Bovine serum albumin-glucose (BSA-glucose) and bovine serum albumin-methylglyoxal (BSA-MGO). The most potent glycation inhibitors, according to the BSA-MGO assay, were star anise (88%), cinnamon (85%), allspice (81%), and cloves (79%), whereas in the BSA-glucose measurement, oregano was noted to be a very effective inhibitor of the glycation process. The ability to inhibit glycation was highly correlated with TP values in the BSA-MGO and BSA-glucose assay (r = 0.84 and 0.76, respectively). Our research showed the high antiglycation ability of cinnamon, cloves, and allspice, and we suggest, for the first time, that anise could also be considered a good glycation inhibitor.
9
Rahbar, Samuel, i James L. Figarola. "Novel inhibitors of advanced glycation endproducts". Archives of Biochemistry and Biophysics 419, nr 1 (listopad 2003): 63–79. http://dx.doi.org/10.1016/j.abb.2003.08.009.
Pełny tekst źródła
10
Rahbar, Samuel, Kiran Kumar Yernini, Stephen Scott, Noe Gonzales i Iraj Lalezari. "Novel Inhibitors of Advanced Glycation Endproducts". Biochemical and Biophysical Research Communications 262, nr 3 (wrzesień 1999): 651–56. http://dx.doi.org/10.1006/bbrc.1999.1275.
Pełny tekst źródłaRozprawy doktorskie na temat "Glycation inhibitors"
1
Gao, Hong Ying 1967. "Assessing the potential of carboxylic acids as inhibitors of glycation". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116072.
Pełny tekst źródłaStreszczenie:
Glycation is a series of chemical interactions occurring in food and biological systems between reducing sugars and proteins leading to the formation of Advanced Glycation End products (AGEs). Ingestion of dietary AGEs and/or their formation in-vivo are mainly associated with cardiovascular and other age-related diseases and complications of long term diabetes. Potential strategies to prevent AGE formation can help to reduce risk factors associated with thermal processing of many foods. The overall objective of this research was focused on the identification of potential AGE inhibitors and investigation of their activity in glucose and ribose-based model systems containing lysozyme. The carboxylic acid functional group was chosen as a potential candidate based on their ability to interact with Schiff bases in addition to their ability to form amide bonds and carboxylate salts with the lysine side chains of proteins. The model systems were incubated with and without selected carboxylic acids (maleic, acetic, oxalic and citraconic) at 50°C for 12, 24 and 48h at pH 6.5. The effect of carboxylic acids on the glycation of lysozyme was studied by electrospray ionization mass spectrometry (ESI-MS). The experimental results showed that none of the carboxylic acids were able to form amide linkages with lysozyme under the experimental conditions and only maleic acid was able to form carboxylate salts, however, oxalic acid was the only acid able to interact with the Schiff base and form 1,3-oxazolidine-4,5-dione intermediate and thus hinder its rearrangement into Amadori product and consequently inhibit glycation. As a result the percentage of free or unreacted lysozyme was the highest in oxalic acid model systems (9.4% in the case of glucose, 7.1% in the case of ribose system) and was even higher than the control systems (6.0% in the case of glucose, 1.2% in the case of ribose system) of both glucose and ribose. In addition, all carboxylic acids were able to modify the relative distribution of different glycoforms generated during the incubation period however oxalic acid was the most efficient in shifting the distribution of glycoforms to lower molecular weight clusters which can additionally contribute to its anti-glycation activity.
2
Peng, Xiaofang, i 彭晓芳. "Naturally occurring inhibitors against the formation of advanced glycation endproducts". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44892706.
Pełny tekst źródła
3
Liebisch, Marita [Verfasser], Gunter [Akademischer Betreuer] Wolf, Tilmann [Akademischer Betreuer] Grune i Thomas [Akademischer Betreuer] Benzing. "Der Einfluss von advanced glycation end-products auf die podozytäre Expression des nuklearen Inhibitors der Proteinphosphatase 1 / Marita Liebisch. Gutachter: Gunter Wolf ; Tilmann Grune ; Thomas Benzing". Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2014. http://d-nb.info/104757912X/34.
Pełny tekst źródła
4
Seidowski, Anne. "Enzymatischer Abbau von Amadori-Produkten durch intestinale Disaccharidasen und intrazelluläre Ketosaminkinasen". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-64960.
Pełny tekst źródłaStreszczenie:
Amadori-Produkte werden spontan während der ersten Phase der Maillard-Reaktion aus reduzierenden Zuckern und Aminen wie Lysin gebildet. Sie entstehen während der Erhitzung von Lebensmitteln und in vivo. Der enzymatische Abbau solcher spontan gebildeten Produkte ist Thema dieser Arbeit. Ein Teil untersuchte die Rolle von Oligosaccharid-Amadori-Produkten während der Verdauung von Kohlenhydraten im Dünndarm. Aufgrund ihrer strukturellen Ähnlichkeit mit bekannten Glycosidase-Inhibitoren wurde eine hemmende Wirkung der Amadori-Produkte auf die Kohlenhydratverdauung vermutet. Der andere Teil beschäftigte sich mit Fructosamin-3-kinase (FN3K) und dessen verwandtem Enzym Fructosamin-3-kinase-related Protein (FN3K-RP) aus humanen Erythrocyten. Diese Ketosaminkinasen werden als Proteinreparaturenzyme betrachtet, sogar als enzymatische Verteidigung gegen Glykierung in vivo diskutiert. Durch ihre Reaktion entstehen jedoch auch hoch-reaktive 1,2-Dicarbonylverbindungen, die weitere Proteinschäden bewirken können. Noch ist nicht klar, ob die Ketosaminkinasen die pathophysiologischen Folgen der Glykierung verhindern oder fördern. In dieser Arbeit wurde die Substratspezifität von Ketosaminkinasen mit einer Reihe von Amadori-Produkten untersucht. Damit könnten Inhibitoren zur weiteren Enzymcharakterisierung oder sogar für pharmazeutische Anwendungen identifiziert werden. Außerdem wurde die Variabilität der Enzymaktivitäten von Mensch zu Mensch in einer Kohorte von 100 Probanden untersucht. Als Modell für die menschliche Kohlenhydratverdauung im Dünndarm wurden Caco-2-Zellen als Monolayer etabliert. Deren Sucrase-Isomaltase kann die alpha-glycosidische Bindung in Amadori-Produkten von Maltose und Maltotriose mit Lysin und auch in Maltulose hydrolysieren. Trotz der Aminogruppe hemmen diese Amadori-Produkte die Maltosehydrolyse nur schwach als konkurrierende Substrate. Lactulosyllysin konnte nicht durch die Lactase der Caco-2-Zellen hydrolysiert werden. Tagatosyllysin und die Heyns-Produkte Glucosyllysin und Mannosyllysin hemmten die Lactosehydrolyse schwach. Alle beobachteten Hemmeffekte sind wahrscheinlich zu schwach, um während der Verdauung in vivo bedeutsam zu sein. Für FN3K konnte Desoxypiperidinofructose als kompetitiver Inhibitor identifiziert werden (Kic 0,006 mM). FN3K zeigte nur geringe Selektivität gegenüber Amadori-Produkten verschiedener Amine, ausgenommen aromatischer Amine. FN3K-RP war in Erythrocyten wesentlich aktiver als FN3K, auch wenn die Aktivität nicht selektiv inhibiert werden konnte. Beide Enzymaktivitäten unterscheiden sich unter den 100 Probanden, mit einer Spannweite von 3 bis 12 mU/g Hämoglobin für FN3K und 60 bis 135 mU/g Hb für FN3K und FN3K-RP zusammen. Es scheint eine Verbindung zwischen der Ketosaminkinase-Aktivität in Erythrocyten und Nierenerkrankungen, familiär auftretendem Diabetes mellitus, sowie familiär aufgetretenen Herzinfarkten oder Schlaganfällen zu bestehen, wie orientierende Auswertungen zeigten. Deshalb ist eine genauere Untersuchung der physiologischen Bedeutung der Ketosaminkinasen nötigAmadori products are formed spontaneously from reducing sugars and amines, e.g. lysine, during the first phase of the Maillard reaction. They occur in heated food and in vivo. The thesis focuses on the enzymatic degradation of such spontaneously formed compounds. One part of this work investigated the faith and impact of oligosaccharide derived Amadori products during small intestinal carbohydrate digestion. Due to their structural similarity with known glycosidase inhibitors, an inhibitory action of Amadori products towards carbohydrate digestions was assumed. The other part dealt with fructosamine-3-kinase (FN3K) and its related protein (FN3K-RP) from human erythrocytes. Such ketosamine kinases are regarded as protein repair enzymes, maybe even an enzymatic defence against glycation in vivo. While deglycating protein bound Amadori products, however, they produce highly reactive 1,2-dicarbonyl compounds, which can lead to further protein damage. It is unclear, whether the ketosamine kinase action prevents or supports the pathophysiological effects of glycation. This work studied the substrate specifity of ketosamine kinases with a variety of Amadori products, which could result in inhibitors for further enzyme characterisation or even pharmaceutical uses. Further, the variability of both enzyme activities in a cohort of 100 subjects was examined. As a model for human small intestinal carbohydrate digestion, a Caco-2 cell monolayer was employed. Their sucrase-isomaltase is able to hydrolyse the alpha-glucosidic linkage in Amadori products of maltose and maltotriose with lysine, as well as in maltulose. Despite their amino group, those amadori products inhibited maltose hydrolysis merely weakly as competing substrates. Lactulosyl lysine on the other hand could not be hydrolysed by Caco-2 lactase. Tagatosyl lysine and the Heyns products glucosyl lysine and mannosyl lysine showed weak inhibition of lactose hydrolysis. All observed inhibitory effects are probably too weak to be of importance during carbohydrate digestion in vivo. Deoxypiperidinofructose was identified as a competitive inhibitor of FN3K (Kic 0,006 mM). FN3K acted rather non-specific towards Amadori products of different amines, except aromatic amines. FN3K-RP showed much higher activity in erythrocytes than FN3K, although its activity could not be inhibited selectively. Both enzyme activities vary among 100 subjects, with a range of 3 to 12 mU/g hemoglobin for FN3K and 60 to 135 mU/g hb for FN3K and FN3K-RP together. Relations of ketosamine kinase activity in erythrocytes with renal diseases, familial diabetes mellitus and familial cardiovascular events seem to exist. Thus, investigating the physiological impact of ketosamine kinases is necessary
5
Brindisi, Marie-Claude. "Relaxation vasculaire et HDL : rôle de la glycation et de l'oxydation des HDL sur la capacité de ces HDL à contrecarrer les effets inhibiteurs des LDL oxydées sur la vasorelaxation endothélium-dépendante". Thesis, Dijon, 2012. http://www.theses.fr/2012DIJOMU05.
Pełny tekst źródłaStreszczenie:
Contrairement aux HDL de sujets sains, les HDL de patients diabétiques ont perdu leur capacité à contrecarrer les effets inhibiteurs des LDL oxydées sur la vasorelaxation endothélium dépendante. Les mécanismes en cause ne sont pas connus. Or la glycation et l’oxydation sont deux phénomènes majeurs au cours du diabète. Nous avons donc étudié in vitro, le rôle de la glycation (associée ou non à une oxydation spontanée), et de l’oxydation d’HDL issues de sujets sains, sur leurs capacités à contrecarrer les effets inhibiteurs des LDL oxydées sur la vasorelaxation endothélium dépendante. Chaque condition a conduit au même constat: les HDL modifiées perdent leur pouvoir vasorelaxant en présence de LDL oxydées. En revanche, en l’absence de LDL oxydées, elles n’altèrent pas la vasorelaxation induite par l’acétylcholine. Ainsi les modifications structurelles des HDL (glycation, oxydation, ou les deux) induisent une perte de leur capacité à protéger l’endothélium du stress oxydatif, plutôt qu’un effet délétère direct sur l’endothélium. Un des mécanismes majeur impliqué dans ce phénomène est probablement l’absence de fixation de ces HDL modifiées à leur récepteur SR-BI. Elles ne pourraient plus alors s’opposer au niveau des cavéoles aux effets délétères des LDL oxydées, et ne favoriseraient plus la production de NO. Mais si aussi bien la glycation que l’oxydation des HDL entraînent ces effets néfastes, il semblerait qu’en condition physiopathologique (oxydation spontanée des HDL glyquées), l’oxydation ne majore pas cette perte de capacité des HDL à contrecarrer les effets inhibiteurs des LDL oxydées sur la vasorelaxationContrary to HDL from normolipidaemic and normoglycaemic subjects, HDL from diabetic patients have lost their capacity to reverse the inhibition of vasorelaxation induced by oxidized LDL. Mechanisms involved are unknown. The glycation and oxidation of HDL are two major phenomena in diabetes mellitus. The aim of this work was to study in vitro the role of glycation (with or without spontaneous oxidation) and oxidation of HDL, on their capacity to counteract the inhibitory effect of oxidized LDL on endothelium-dependent vasorelaxation. Each state showed the same result, modified HDL lost their vasorelaxing power in stress conditions (with oxidized LDL). Nevertheless, modified HDL alone (without oxidized LDL) did not alter vasorelaxation induced by acetylcholine, after noradrenaline-induced vasoconstriction. Thus, modifications of HDL induce a loss of the ability to protect vessels from oxidative stress rather than have a direct deleterious effect on the vessel. One of the major mechanisms involved in this phenomenon is probably the loss of SR-BI binding of these modified HDL, that could lead to the inability of HDL to protect caveolae from deleterious effects induced by oxidized LDL and could not preserve NO production. However, though glycation, like oxidation of HDL, leads to these deleterious effects, it would seem that during physiopathological conditions, with the spontaneous oxidation of glycated HDL, oxidation does not aggravate the loss of the capacity of diabetic HDL to counteract the inhibitory effect of oxidized LDL on endothelium-dependent vasorelaxation
6
Mooney, Mark Hugh. "Glucagon like peptide 1 and gastric inhibitory polypeptide : effects of N terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity". Thesis, University of Ulster, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268580.
Pełny tekst źródła
7
Younessi, Parisa. "Effect of glycated proteins and inhibitory compounds intervening with the AGE-RAGE pathway on macrophages". Thesis, 2010. http://handle.uws.edu.au:8081/1959.7/498349.
Pełny tekst źródłaStreszczenie:
Glycation is a specific type of protein modification in ageing. The reaction of reducing sugar with a primary amino group is the most common nonenzymatic modification of proteins. Subsequent rearrangement, oxidation and dehydration yield a heterogeneous group of mostly coloured and fluorescent compounds, termed “Maillard products” or “advanced glycation end products (AGEs)”. AGEs are thought to play a role in the aetiology of various age-related diseases such as diabetes mellitus (DM) and Alzheimer's disease (AD). AD is a multifactorial disease, in which the rate of synapse loss and neuronal cell death determines the onset and/or progression of dementia. Activation of microglia and astrocytes with subsequent oxidative stress and cytokine release may be an important progression factor for AD. It is also suggested that the receptor for advanced glycation end products (RAGE) ligands-AGEs interaction might be another cause of glial activation, cytokine and reactive oxygen species (ROS) release. Different antioxidants, receptor mediated compounds and ROS scavenging enzymes might be able to intervene with the AGE-RAGE signalling pathway and slow down the progression of AD. The aim of this study is to investigate the effect of different compounds of antioxidants, receptor mediated compounds and ROS scavenging enzymes on inflammation induced by glycated proteins and to explore the suggested AGE-RAGE signalling pathway by examining inhibition of different parts of the signalling network.
8
Seidowski, Anne. "Enzymatischer Abbau von Amadori-Produkten durch intestinale Disaccharidasen und intrazelluläre Ketosaminkinasen: Enzymatic degradation of Amadori products by intestinal disaccharidases and intracellular ketosamine kinases". Doctoral thesis, 2010. https://tud.qucosa.de/id/qucosa%3A25500.
Pełny tekst źródłaStreszczenie:
Amadori-Produkte werden spontan während der ersten Phase der Maillard-Reaktion aus reduzierenden Zuckern und Aminen wie Lysin gebildet. Sie entstehen während der Erhitzung von Lebensmitteln und in vivo. Der enzymatische Abbau solcher spontan gebildeten Produkte ist Thema dieser Arbeit.
Ein Teil untersuchte die Rolle von Oligosaccharid-Amadori-Produkten während der Verdauung von Kohlenhydraten im Dünndarm. Aufgrund ihrer strukturellen Ähnlichkeit mit bekannten Glycosidase-Inhibitoren wurde eine hemmende Wirkung der Amadori-Produkte auf die Kohlenhydratverdauung vermutet. Der andere Teil beschäftigte sich mit Fructosamin-3-kinase (FN3K) und dessen verwandtem Enzym Fructosamin-3-kinase-related Protein (FN3K-RP) aus humanen Erythrocyten. Diese Ketosaminkinasen werden als Proteinreparaturenzyme betrachtet, sogar als enzymatische Verteidigung gegen Glykierung in vivo diskutiert. Durch ihre Reaktion entstehen jedoch auch hoch-reaktive 1,2-Dicarbonylverbindungen, die weitere Proteinschäden bewirken können. Noch ist nicht klar, ob die Ketosaminkinasen die pathophysiologischen Folgen der Glykierung verhindern oder fördern. In dieser Arbeit wurde die Substratspezifität von Ketosaminkinasen mit einer Reihe von Amadori-Produkten untersucht. Damit könnten Inhibitoren zur weiteren Enzymcharakterisierung oder sogar für pharmazeutische Anwendungen identifiziert werden. Außerdem wurde die Variabilität der Enzymaktivitäten von Mensch zu Mensch in einer Kohorte von 100 Probanden untersucht.
Als Modell für die menschliche Kohlenhydratverdauung im Dünndarm wurden Caco-2-Zellen als Monolayer etabliert. Deren Sucrase-Isomaltase kann die alpha-glycosidische Bindung in Amadori-Produkten von Maltose und Maltotriose mit Lysin und auch in Maltulose hydrolysieren. Trotz der Aminogruppe hemmen diese Amadori-Produkte die Maltosehydrolyse nur schwach als konkurrierende Substrate. Lactulosyllysin konnte nicht durch die Lactase der Caco-2-Zellen hydrolysiert werden. Tagatosyllysin und die Heyns-Produkte Glucosyllysin und Mannosyllysin hemmten die Lactosehydrolyse schwach. Alle beobachteten Hemmeffekte sind wahrscheinlich zu schwach, um während der Verdauung in vivo bedeutsam zu sein.
Für FN3K konnte Desoxypiperidinofructose als kompetitiver Inhibitor identifiziert werden (Kic 0,006 mM). FN3K zeigte nur geringe Selektivität gegenüber Amadori-Produkten verschiedener Amine, ausgenommen aromatischer Amine. FN3K-RP war in Erythrocyten wesentlich aktiver als FN3K, auch wenn die Aktivität nicht selektiv inhibiert werden konnte. Beide Enzymaktivitäten unterscheiden sich unter den 100 Probanden, mit einer Spannweite von 3 bis 12 mU/g Hämoglobin für FN3K und 60 bis 135 mU/g Hb für FN3K und FN3K-RP zusammen. Es scheint eine Verbindung zwischen der Ketosaminkinase-Aktivität in Erythrocyten und Nierenerkrankungen, familiär auftretendem Diabetes mellitus, sowie familiär aufgetretenen Herzinfarkten oder Schlaganfällen zu bestehen, wie orientierende Auswertungen zeigten. Deshalb ist eine genauere Untersuchung der physiologischen Bedeutung der Ketosaminkinasen nötig.Amadori products are formed spontaneously from reducing sugars and amines, e.g. lysine, during the first phase of the Maillard reaction. They occur in heated food and in vivo. The thesis focuses on the enzymatic degradation of such spontaneously formed compounds. One part of this work investigated the faith and impact of oligosaccharide derived Amadori products during small intestinal carbohydrate digestion. Due to their structural similarity with known glycosidase inhibitors, an inhibitory action of Amadori products towards carbohydrate digestions was assumed. The other part dealt with fructosamine-3-kinase (FN3K) and its related protein (FN3K-RP) from human erythrocytes. Such ketosamine kinases are regarded as protein repair enzymes, maybe even an enzymatic defence against glycation in vivo. While deglycating protein bound Amadori products, however, they produce highly reactive 1,2-dicarbonyl compounds, which can lead to further protein damage. It is unclear, whether the ketosamine kinase action prevents or supports the pathophysiological effects of glycation. This work studied the substrate specifity of ketosamine kinases with a variety of Amadori products, which could result in inhibitors for further enzyme characterisation or even pharmaceutical uses. Further, the variability of both enzyme activities in a cohort of 100 subjects was examined. As a model for human small intestinal carbohydrate digestion, a Caco-2 cell monolayer was employed. Their sucrase-isomaltase is able to hydrolyse the alpha-glucosidic linkage in Amadori products of maltose and maltotriose with lysine, as well as in maltulose. Despite their amino group, those amadori products inhibited maltose hydrolysis merely weakly as competing substrates. Lactulosyl lysine on the other hand could not be hydrolysed by Caco-2 lactase. Tagatosyl lysine and the Heyns products glucosyl lysine and mannosyl lysine showed weak inhibition of lactose hydrolysis. All observed inhibitory effects are probably too weak to be of importance during carbohydrate digestion in vivo. Deoxypiperidinofructose was identified as a competitive inhibitor of FN3K (Kic 0,006 mM). FN3K acted rather non-specific towards Amadori products of different amines, except aromatic amines. FN3K-RP showed much higher activity in erythrocytes than FN3K, although its activity could not be inhibited selectively. Both enzyme activities vary among 100 subjects, with a range of 3 to 12 mU/g hemoglobin for FN3K and 60 to 135 mU/g hb for FN3K and FN3K-RP together. Relations of ketosamine kinase activity in erythrocytes with renal diseases, familial diabetes mellitus and familial cardiovascular events seem to exist. Thus, investigating the physiological impact of ketosamine kinases is necessary.
9
Lin, Jin-Yan, i 林晉延. "Studies on inhibitory activity of carbohydrate hydrolyzing enzymes and glycation products of passion fruit seed ethanol extracts". Thesis, 2018. http://ndltd.ncl.edu.tw/handle/926mqp.
Pełny tekst źródłaStreszczenie:
碩士國立嘉義大學
食品科學系研究所
106
In this study, passion fruit seeds were employed as the raw materials, and four different concentrations of ethanol (25/50/75/95%) were used as extraction solvents to investigate the antioxidant activity, blood glucose reduction activity and anti-glycation activities of extracts and functional compounds from extracts. The results showed that the solid yield of extract which used 75% ethanol as the extraction solvent for 24 hours normal temperature extraction of the passion fruit seed (PSE75) is about 3.62 ± 0.23 (%), which is 0.52 times the 50% ethanol extract (PSE50). However, the PSE75 contained higher phenolic compounds content and antioxidant activity. The total phenolic compound content, flavonoid compound content, total antioxidant capacity and DPPH free radical scavenging capacity were were 3.9, 3.8, 1.9, 2.7 times the PSE50. In addition, HPLC analysis result that the main functional compound of the ethanol extract was piceatannol (PI). PSE75 contained the highest piceatannol (88.37 ± 5.66 (mg PI/g extract)) among the extracts. The result of α-amylase and α-glucosidase inhibitory activity demonstrated that PSE75 showed the better half-inhibitory activity (IC50), with 188.1 and 3.3 (ppm), respectively, indicating that PSE75 possessed high inhibitory activity. PI and acarbose standard were used to conduct α-glucosidase inhibitory activity assay, the results displayed that IC50 of PI and Acarbose were lower than PSE 75 with 10.5 (ppm) and 816.3 (ppm), respectively. Therefore, passion fruit seeds demonstrated the blood glucose reduction activity. The anti-glycation activity of passion fruit seeds was investigated via determine the methylglyoxal trapping activity and the inhibitory activity on primary, middle and end products in Glucose-BSA and Fructose-BSA glycation systems of samples. The results showed that PSE75 had the best methylglyoxal capture ability and could inhibit the production of primary, middle and final products in the two glycation system among the different extracts. In addition, after glycation incubation with PI standards, the results showed that the production of fluorescent products was higher than the glycation control group, and the lower the standard concentration, the higher the production of fluorescent products. In SDS-PAGE electrophoresis assay, the PSE75-treated group produced an additional non-glycosylated protein at 97 kda, and the staining intensity was higher than high-molecular-weight glycated protein produced in the glycaction control group at a similar molecular weight. In addition, the electrophoresis profile of the PI standard product treatment group also produced non-glycosylated protein at a molecular weight of 97 kda, and the formation of additional non-glycosylated proteins was also observed at higher molecular weights. Therefore, it is speculated that PI could interact with glycosylation sites intermolecularly on BSA by hydrogen bond to generate a transition product with fluorescent properties and other high-molecule crosslinked product. Through the blocking of glycosylation site to prevent the glycation damage caused by the reducing sugars in the hyperglycemic state.
10
Lin, Jer-An, i 林哲安. "Assessing effects of methylglyoxal on colon cancer development and inhibitory effects of breadfruit flavonoid derivatives on advanced glycation end products-enhanced colon malignancy". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/79611049779463404091.
Pełny tekst źródłaStreszczenie:
博士國立中興大學
食品暨應用生物科技學系所
103
The incidence and mortality of colon cancer have been increasing over the past few decades. Epidemiological statistics reveal that the change in the dietary style is closely related to this trend. Therefore, effects of advanced glycation end products (AGEs) and methylglyoxal (MG; a precursor of AGEs), which are known as Maillard reaction products with pro-carcinogenic activity (pro-oxidant and pro-inflammatory activities) found in common processed foods, on colon cancer development are assessed in this study. Additionally, as dietary control may be a good strategy for colon cancer prevention, the present study further evaluated inhibitory effects of flavonoids (polyphenols with cancer-preventive potential in natural source) on AGEs-enhanced malignancy of colon cancer cells. There are three topics included in the thesis, and these topics are described as follows: Chapter 1 was designed to assess the effect of MG on colon cancer development. The result of azoxymethane (AOM)-induced animal test indicated that consumption of MG (1% in drinking water) can significantly promote the development of colonic preneoplastic lesions in AOM-induced ICR mice, in which increased pro-oxidants and pro-inflammatory substances within body and feces may play important roles. Furthermore, the result of CT26 colon tumor-bearing animal test showed that MG could increase the protein expression of the receptor for AGEs (RAGE) which has been demonstrated as the important mediator in the process of pro-carcinogenic inflammation and IL-6 levels. Also, MG could enhance CT26 colon tumor growth and increase the degree of malignancy of related primary tumor cells, as well as enhance expression or activation of proteins (GLO1/2、ERK/p38 MAPK、PI3K/mTOR、SIRT1、vimentin) that modulate survival, proliferation or migration/invasion in those primary tumor cells. However, N-acetylcysteine (NAC, 150 mg/kg b.w.; p.o.), a MG scavenger with antioxidant property, may ameliorate the impact of MG on tumor-bearing BALB/c mice as just mentioned, while alagebrium chloride (ALA, 1 mg/kg b.w.; p.o.), a MG scavenger and AGEs crosslink breaker, only partially reduced MG-elevated degree of malignancy of primary tumor cells. Chapter 2 was to investigate whether flavonoid derivatives isolated from the fruit of Artocarpus communis (breadfruit) (i.e., breadfruit flavonoid derivatives) could decrease the inflammatory response induced by S100B, a ligand of the receptor for AGEs (RAGE) in the human THP-1 monocytes (THP-1 monocytes). Result showed that S100B-induced THP-1 monocytes exhibited the morphological characteristics of inflammation, which were inhibited by the addition of breadfruit flavonoid derivatives. Moreover, breadfruit flavonoid derivatives can inhibit S100B-induced reactive oxygen species (ROS) generation, mRNA expression of pro-inflammatory mediators, and secretion of pro-inflammatory mediators. To clarify the underlying mechanism, breadfruit flavonoid derivatives were shown to attenuate the expression or the activity of the key mediators in RAGE-dependent signaling pathway, including expression of PKC and p47phox, phosphorylation of ERK and p38 MAPK, and particularly NF-κB activation. Therefore, breadfruit flavonoid derivatives could ameliorate RAGE-mediated inflammatory response. Chapter 3 was to investigate effects of breadfruit flavonoid derivatives on AGEs-enhanced colon malignancy in vitro. Results showed that glyceraldehyde-derived AGEs can increase the degree of malignancy of HCT116 colon cancer cells (HCT116 cells) by activating RAGE-dependent signaling pathway, while breadfruit flavonoid derivatives may attenuate the impact of these AGEs on the malignancy of HCT116 cells. Additionally, the mechanisms underlying AGEs-evoked responses, including activation of MAPK/NF-κB cascades and translocation of STAT3 and β-catenin were ameliorated with different degrees by breadfruit flavonoid derivatives individually. Furthermore, we first found that breadfruit flavonoid derivatives can inhibit the proliferation of HCT116 cells induced by conditioned media from AGEs-induced THP-1 monocytes, which may be closely related to anti-inflammatory features of breadfruit flavonoid derivatives. In conclusion, the present study indicates that MG, a precursor of AGEs, can promote colon cancer progression through increasing oxidative stress, inflammation-associated cytokines and the modulator in the process of pro-carcinogenic inflammation (i.e., RAGE), and AGEs per se can increase the degree of malignancy of colon cancer cells through ligation of RAGE. Additionally, breadfruit flavonoid derivatives have potent inhibitory effect on RAGE-mediated inflammatory responses in vitro and on AGEs/RAGE-enhanced malignancy of colon cancer cells. These promising results can provide a new insight into the pathological role of MG and AGEs in colon tumorigenesis, and flavonoid-like compounds of breadfruit may have potent implications to repress colon cancer progression.
Książki na temat "Glycation inhibitors"
1
Mooney, Mark H. Glucagon-like peptide-1 and gastric inhibitory polypeptide: Effects of N-terminal glycation on hormone degradation, insulin secretion and antihyperglycaemic activity. [S.l: The Author], 2000.
Znajdź pełny tekst źródła
2
Chong, Sandra Ann Chen. Diabetes induced glycation of collagen inhibits the binding step of collagen phagocytosis. 2006.
Znajdź pełny tekst źródłaCzęści książek na temat "Glycation inhibitors"
1
Farris, Patricia K. "Skin Aging, Glycation and Glycation Inhibitors". W Cosmeceuticals and Cosmetic Practice, 173–83. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118384824.ch17.
Pełny tekst źródła
2
Dayal, Bishambar, Vineela Reddy Yannamreddy, Ajay P. Singh, Michael Lea i Norman H. Ertel. "Bioactive Compounds from Okra Seeds: Potential Inhibitors of Advanced Glycation End Products". W ACS Symposium Series, 287–302. Washington, DC: American Chemical Society, 2012. http://dx.doi.org/10.1021/bk-2012-1093.ch016.
Pełny tekst źródła
3
Dan, Takashi, Charles van Ypersele de Strihou i Toshio Miyata. "Advanced Glycation End Products Inhibitor". W Studies on Renal Disorders, 389–406. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-857-7_20.
Pełny tekst źródła
4
Kageyama, Hakuto. "Biological Activities of MAAs and their Applications 4: Anti-glycative Properties". W An Introduction to Mycosporine-Like Amino Acids, 94–101. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815136081123010010.
Pełny tekst źródłaStreszczenie:
Advanced glycation end products (AGEs) are formed by a series of chemical reactions initiated by non-enzymatic glycation reactions. In this process, the reducing sugar binds to the free amino group of the protein. The formation of AGEs that accompany the aging process is thought to be associated with various diseases such as diabetes and Alzheimer's disease. A number of inhibitors derived from synthetic compounds and natural products have been developed and evaluated to prevent the formation of AGEs. Compared to synthetic compounds, natural products are considered to be relatively safe for human consumption, so there is an increasing demand for compounds derived from natural products. From this perspective, this chapter focuses on mycosporine-like amino acids as naturally occurring inhibitors against AGEs formation.
5
Inagi, Reiko. "Inhibitors of Advanced Glycation and Endoplasmic Reticulum Stress". W Methods in Enzymology, 361–80. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-385928-0.00020-1.
Pełny tekst źródła
6
Sourris, Karly C., Anna Watson i Karin Jandeleit-Dahm. "Inhibitors of Advanced Glycation End Product (AGE) Formation and Accumulation". W Handbook of Experimental Pharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/164_2020_391.
Pełny tekst źródła
7
Khan, Rujman, Xin Yee Ooi, Matthew Parvus, Laura Valdez i Andrew Tsin. "Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications". W The Eye and Foot in Diabetes. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89408.
Pełny tekst źródłaStreszczenie:
Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
8
Kageyama, Hakuto. "Biological Activities of MAAs and their Applications 6: Metal Chelating Abilities". W An Introduction to Mycosporine-Like Amino Acids, 107–10. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815136081123010012.
Pełny tekst źródłaStreszczenie:
As mentioned in Chapters 8 and 9, the useful functions of MAAs, such as the anti-glycative property and collagenase inhibitory activity, might be associated with their metal chelating activity. Although there are few reports on the metal-chelating activity of MAAs, a chelating model of MAAs and metal ions has recently been proposed. This chapter briefly summarizes these observations.
9
Kinae, Naohida, Masanori Matsuda, Mutuo Shigeta i Kayoko Shimoi. "Inhibitory Effect of Polei Tea Extract on the Formation of Advanced Glycation Endproducts in Vivo". W The Maillard Reaction in Foods and Medicine, 416. Elsevier, 2005. http://dx.doi.org/10.1533/9781845698447.8.416a.
Pełny tekst źródłaStreszczenia konferencji na temat "Glycation inhibitors"
1
Hartmann, A., M. Orfanoudaki, P. Blanchard, S. Derbre, A. Schinkovitz, P. Richomme, M. Ganzera i H. Stuppner. "Secondary metabolites from marine sources as inhibitors of advanced glycation end products (AGEs) and collagenase". W 67th International Congress and Annual Meeting of the Society for Medicinal Plant and Natural Product Research (GA) in cooperation with the French Society of Pharmacognosy AFERP. © Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-3400086.
Pełny tekst źródła
2
Rana, S., M. G. Tonnesen, X.-D. Ren i R. A. Clark. "Early glycation of critical fibronectin domains inhibits human dermal fibroblast migration". W 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413357.
Pełny tekst źródła
3
Shah Muhammad, A., H. Muhammad, R. Khalil, Z. Ul-Haq i P. Panichayupakaranant. "Rhinacanthins-rich extract: A potent superoxide scavenger and advanced glycation end-product formation inhibitor". W GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608423.
Pełny tekst źródła
4
Ansari, Prawej, JM A. Hannan, Yasser H. A. Abdel-Wahab i Peter R. Flatt. "Antidiabetic and insulinotropic properties of bark of Heritiera fomes: inhibits starch digestion, protein glycation, DPP-IV activity, and glucose absorption in gut." W GA – 69th Annual Meeting 2021, Virtual conference. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736789.
Pełny tekst źródła
5
Dwiwibangga, Yoravika, Fatchiyah i Anna Safitri. "In silico analysis reveals the potential of myricetin of red rice bran east java as inhibitor for the advanced glycation end products (AGEs)-Receptor (RAGE) signaling pathway". W THE PROCEEDINGS OF THE 4TH EPI INTERNATIONAL CONFERENCE ON SCIENCE AND ENGINEERING (EICSE) 2020. AIP Publishing, 2022. http://dx.doi.org/10.1063/5.0099247.
Pełny tekst źródła