Comparative Study on the Status of Glycation Precursors, Advanced Glycation End Products, and Cell Viability Under Effects of Kaempferol, Myricetin, and Azaleatin in HGC-27 Cell Line

Journal of young investigators Pub Date : 2019-01-01 DOI:10.22186/jyi.36.1.5-10

Fargol Ma Boojar, Sepideh Golmohamad, G. Tafreshi

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Abstract

rosis, and Alzheimer’s Disease (Hartog et al., 2007; Reddy and Obrenovich, 2002). However, in response to increased glycation, some of the accumulated glycation adducts may be omitted by enzymatic repair mechanisms while others are degraded by proteases (Vander and Hunsaker, 2003; Nemet et al., 2006). The major contributing molecules with different potentials to form AGEs are 3-deoxyglucoson, glyoxal, pentosidine, and methylglyoxal. 3-Deoxyglucosone (3-DG) is a highly reactive dicarboxyl sugar and a precursor for AGE generation by cells, particularly when excessive glucose is taken up or when a person is diabetic. In addition, it can damage some antioxidant enzymes such as glutathione reductase, which is inactivated by excess 3-deoxyglucosone (Tauer et al., 2001; Schalwijk et al., 1999). On the other hand, pentosidine is a fluorescent molecule and represents an adequate and sensitive marker for all AGEs within cells. It is an imidazole [4,5b] pyridinum ring formed by cross linking between lysine and arginine residues (Dyer et al., 1991; Spacek and Adam, 2002). The elevation of pentosidine is associated with ageing and related complications, including cartilage stiffness and damage that causes physical disability (Senolt et al., 2005; Verzijl et al., 2002). Glyoxal may be formed via autoxidation and spontaneous degradation of glucose by retro-aldol condensation under physiological conditions (Paul et al., 1999). The methylated form of this compound, methylglyoxal, can be produced by fragmentation of 3-deoxyglucosone and is also a byproduct of glycolysis and amino acid catabolism (Frank et al., 1996). Current knowledge of glycation indicates that it may be an Comparative Study on the Status of Glycation Precursors, Advanced Glycation End Products, and Cell Viability Under Effects of Kaempferol, Myricetin, and Azaleatin in HGC-27 Cell Line

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山奈酚、杨梅素和杜鹃花素对HGC-27细胞株糖基化前体、晚期糖基化终产物及细胞活力的影响

骨质疏松和阿尔茨海默病(Hartog et al.， 2007;Reddy and Obrenovich, 2002)。然而，在糖基化增加的情况下，一些累积的糖基化加合物可能会被酶修复机制所忽略，而另一些则会被蛋白酶降解(Vander和Hunsaker, 2003;Nemet et al.， 2006)。具有不同电位形成AGEs的主要分子是3-脱氧葡萄糖、乙二醛、戊苷和甲基乙二醛。3-脱氧葡萄糖酮(3-DG)是一种高活性的二羧基糖，是细胞生成AGE的前体，特别是当过量的葡萄糖被摄取或当一个人患有糖尿病时。此外，它可以破坏一些抗氧化酶，如谷胱甘肽还原酶，过量的3-脱氧葡萄糖会使谷胱甘肽还原酶失活(Tauer等，2001;Schalwijk et al.， 1999)。另一方面，戊苷是一种荧光分子，代表了细胞内所有AGEs的充分和敏感的标记物。它是赖氨酸和精氨酸残基交联形成的咪唑[4,5b]吡啶环(Dyer et al.， 1991;斯派塞克和亚当，2002)。戊苷的升高与衰老和相关并发症有关，包括导致身体残疾的软骨僵硬和损伤(Senolt等人，2005;Verzijl et al.， 2002)。乙二醛可以在生理条件下通过葡萄糖的自氧化和醛醇缩合自发降解而形成(Paul et al.， 1999)。这种化合物的甲基化形式甲基乙二醛可以通过3-脱氧葡萄糖酮的断裂产生，也是糖酵解和氨基酸分解代谢的副产物(Frank et al.， 1996)。目前对糖基化的研究表明，在山奈酚、杨梅素和氮杂藻素的作用下，糖基化前体、晚期糖基化终产物和HGC-27细胞系细胞活力的状态可能是一项比较研究

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Journal of young investigators

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