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Статті в журналах з теми "Glycation inhibitors"
Perera, HKI, and DCR Wijetunge. "A novel in vitro method to detect inhibitors of protein glycation." Asian Journal of Medical Sciences 5, no. 3 (February 24, 2014): 15–21. http://dx.doi.org/10.3126/ajms.v5i3.8670.
Повний текст джерелаE-FARAN, MISS GULL, MUHAMMAD ANJUM ZIA, and NIGHAT ASLAM. "EFFECT OF CAPTOPRIL." Professional Medical Journal 19, no. 01 (January 3, 2012): 078–85. http://dx.doi.org/10.29309/tpmj/2012.19.01.1929.
Повний текст джерелаPawlukianiec, Cezary, Małgorzata Ewa Gryciuk, Kacper Maksymilian Mil, Małgorzata Żendzian-Piotrowska, Anna Zalewska, and Mateusz Maciejczyk. "A New Insight into Meloxicam: Assessment of Antioxidant and Anti-Glycating Activity in In Vitro Studies." Pharmaceuticals 13, no. 9 (September 10, 2020): 240. http://dx.doi.org/10.3390/ph13090240.
Повний текст джерелаWest, Brett J., Shixin Deng, Akemi Uwaya, Fumiyuki Isami, Yumi Abe, Sho-ichi Yamagishi, and C. Jarakae Jensen. "Iridoids are natural glycation inhibitors." Glycoconjugate Journal 33, no. 4 (June 15, 2016): 671–81. http://dx.doi.org/10.1007/s10719-016-9695-x.
Повний текст джерелаHosseini, Asieh, and 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.
Повний текст джерелаJulius, Angeline, and 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, no. 11 (November 1, 2017): 173. http://dx.doi.org/10.22159/ajpcr.2017.v10i11.19412.
Повний текст джерелаPervez, Humayun, Nazia Khan, Jamshed Iqbal, Sumera Zaib, Muhammad Yaqub, Muhammad Nawaz Tahir, and 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, no. 1 (February 23, 2018): 51–58. http://dx.doi.org/10.1515/hc-2017-0148.
Повний текст джерелаStarowicz, Małgorzata, and Henryk Zieliński. "Inhibition of Advanced Glycation End-Product Formation by High Antioxidant-Leveled Spices Commonly Used in European Cuisine." Antioxidants 8, no. 4 (April 15, 2019): 100. http://dx.doi.org/10.3390/antiox8040100.
Повний текст джерелаRahbar, Samuel, and James L. Figarola. "Novel inhibitors of advanced glycation endproducts." Archives of Biochemistry and Biophysics 419, no. 1 (November 2003): 63–79. http://dx.doi.org/10.1016/j.abb.2003.08.009.
Повний текст джерелаRahbar, Samuel, Kiran Kumar Yernini, Stephen Scott, Noe Gonzales, and Iraj Lalezari. "Novel Inhibitors of Advanced Glycation Endproducts." Biochemical and Biophysical Research Communications 262, no. 3 (September 1999): 651–56. http://dx.doi.org/10.1006/bbrc.1999.1275.
Повний текст джерелаДисертації з теми "Glycation inhibitors"
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.
Повний текст джерелаPeng, Xiaofang, and 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.
Повний текст джерелаLiebisch, Marita [Verfasser], Gunter [Akademischer Betreuer] Wolf, Tilmann [Akademischer Betreuer] Grune, and 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.
Повний текст джерелаSeidowski, 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.
Повний текст джерелаAmadori 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
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.
Повний текст джерелаContrary 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
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.
Повний текст джерелаYounessi, 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.
Повний текст джерелаSeidowski, 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.
Повний текст джерелаAmadori 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.
Lin, Jin-Yan, and 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.
Повний текст джерела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.
Lin, Jer-An, and 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.
Повний текст джерела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.
Книги з теми "Glycation inhibitors"
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.
Знайти повний текст джерелаChong, Sandra Ann Chen. Diabetes induced glycation of collagen inhibits the binding step of collagen phagocytosis. 2006.
Знайти повний текст джерелаЧастини книг з теми "Glycation inhibitors"
Farris, Patricia K. "Skin Aging, Glycation and Glycation Inhibitors." In Cosmeceuticals and Cosmetic Practice, 173–83. Chichester, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118384824.ch17.
Повний текст джерелаDayal, Bishambar, Vineela Reddy Yannamreddy, Ajay P. Singh, Michael Lea, and Norman H. Ertel. "Bioactive Compounds from Okra Seeds: Potential Inhibitors of Advanced Glycation End Products." In ACS Symposium Series, 287–302. Washington, DC: American Chemical Society, 2012. http://dx.doi.org/10.1021/bk-2012-1093.ch016.
Повний текст джерелаDan, Takashi, Charles van Ypersele de Strihou, and Toshio Miyata. "Advanced Glycation End Products Inhibitor." In Studies on Renal Disorders, 389–406. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-857-7_20.
Повний текст джерелаKageyama, Hakuto. "Biological Activities of MAAs and their Applications 4: Anti-glycative Properties." In An Introduction to Mycosporine-Like Amino Acids, 94–101. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815136081123010010.
Повний текст джерелаInagi, Reiko. "Inhibitors of Advanced Glycation and Endoplasmic Reticulum Stress." In Methods in Enzymology, 361–80. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-385928-0.00020-1.
Повний текст джерелаSourris, Karly C., Anna Watson, and Karin Jandeleit-Dahm. "Inhibitors of Advanced Glycation End Product (AGE) Formation and Accumulation." In Handbook of Experimental Pharmacology. Berlin, Heidelberg: Springer Berlin Heidelberg, 2020. http://dx.doi.org/10.1007/164_2020_391.
Повний текст джерелаKhan, Rujman, Xin Yee Ooi, Matthew Parvus, Laura Valdez, and Andrew Tsin. "Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications." In The Eye and Foot in Diabetes. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89408.
Повний текст джерелаKageyama, Hakuto. "Biological Activities of MAAs and their Applications 6: Metal Chelating Abilities." In An Introduction to Mycosporine-Like Amino Acids, 107–10. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815136081123010012.
Повний текст джерелаKinae, Naohida, Masanori Matsuda, Mutuo Shigeta, and Kayoko Shimoi. "Inhibitory Effect of Polei Tea Extract on the Formation of Advanced Glycation Endproducts in Vivo." In The Maillard Reaction in Foods and Medicine, 416. Elsevier, 2005. http://dx.doi.org/10.1533/9781845698447.8.416a.
Повний текст джерелаТези доповідей конференцій з теми "Glycation inhibitors"
Hartmann, A., M. Orfanoudaki, P. Blanchard, S. Derbre, A. Schinkovitz, P. Richomme, M. Ganzera, and H. Stuppner. "Secondary metabolites from marine sources as inhibitors of advanced glycation end products (AGEs) and collagenase." In 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.
Повний текст джерелаRana, S., M. G. Tonnesen, X.-D. Ren, and R. A. Clark. "Early glycation of critical fibronectin domains inhibits human dermal fibroblast migration." In 2007 IEEE 33rd Annual Northeast Bioengineering Conference. IEEE, 2007. http://dx.doi.org/10.1109/nebc.2007.4413357.
Повний текст джерелаShah Muhammad, A., H. Muhammad, R. Khalil, Z. Ul-Haq, and P. Panichayupakaranant. "Rhinacanthins-rich extract: A potent superoxide scavenger and advanced glycation end-product formation inhibitor." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608423.
Повний текст джерелаAnsari, Prawej, JM A. Hannan, Yasser H. A. Abdel-Wahab, and 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." In GA – 69th Annual Meeting 2021, Virtual conference. Georg Thieme Verlag, 2021. http://dx.doi.org/10.1055/s-0041-1736789.
Повний текст джерелаDwiwibangga, Yoravika, Fatchiyah, and 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." In 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.
Повний текст джерела