Pharmaceutical intervention of advanced glycation endproducts.

A. Cerami, P. Ulrich
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引用次数: 18

Abstract

Recent studies have revealed that reducing sugars, such as glucose, react with proteins through non-enzymatic glycosylation to form irreversible, covalently cross-linked proteins known as advanced glycation endproducts (AGEs). Furthermore, it has been demonstrated that this naturally occurring process, accelerated in diabetics due to hyperglycaemia, impairs biological functions leading to cardiovascular disorders, as well as diabetic and age-related complications. Pharmaceutical intervention to prevent or reverse these complications have focused on inhibiting the formation of AGEs by compounds such as dimethyl-3-phenacylthiazolium chloride or breaking the glucose derived cross-links by selective cleavage. Intervention targeted at AGE cross-links in vivo offers a way to interfere with age-related changes of tissues.
晚期糖基化终产物的药物干预。
最近的研究表明,还原糖,如葡萄糖,通过非酶糖基化与蛋白质反应,形成不可逆的共价交联蛋白,称为晚期糖基化终产物(AGEs)。此外,已经证明这种自然发生的过程,在糖尿病患者中由于高血糖而加速,损害生物功能,导致心血管疾病,以及糖尿病和与年龄相关的并发症。预防或逆转这些并发症的药物干预主要集中在通过二甲基-3-phenacylthiazolium chloride等化合物抑制AGEs的形成或通过选择性切割破坏葡萄糖衍生的交联。针对AGE交联在体内的干预提供了一种干预与年龄相关的组织变化的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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