晚期糖基化终末产物抗体

产品介绍background:
Advanced Glycation End products (AGEs) are the result of a chain of chemical reactions after an initial glycation reaction. The intermediate products are known, variously, as Amadori, Schiff base and Maillard products, named after the researchers who first described them. (The literature is inconsistent in applying these terms. For example, Maillard reaction products are sometimes considered intermediates and sometimes end products.) Side products generated in intermediate steps may be oxidizing agents (such as hydrogen peroxide), or not (such as beta amyloid proteins).[1] "Glycosylation" is sometimes used for "glycation" in the literature, usually as 'non-enzymatic glycosylation. The AGE modified BSA was produced by reacting BSA with glycolaldehyde under sterile conditions followed by extensive dialysis and purification steps.

Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

AGEs又称非酶糖基化终末产物(AGEs) 是蛋白质、脂质和核酸等大分子的游离氨基与还原性单糖的醛基反应所生成的稳定的共价化合物, 在体内的积累、增多是导致糖尿病等多种疾病及其并发症的关键因素。AGEs的异常增多，可直接或间接地对机体产生致病作用。
晚期糖基化终末产物-AGEs的相关学说
晚期糖基化终末产物（Advanced glycation endproducts，AGEs）是一类经由糖，包括通过Maillard反应形成的代谢中间产物化学修饰的蛋白。AGEs具有高度交联性。 AGE与AGE受体（如RAGE）的相互作用诱导了受体承载细胞核因子-κB（NF—κB）的活化，同时这一作用还诱导了细胞因子、生长因子及黏附分子表达的增加。
在糖尿病方面，晚期糖基化终末产物(AGEs)可引起体内组织一系列病理生理改变,是导致糖尿病慢性并发症的重要致病因素。在健康人群中AGEs也随年龄增加在组织中持续积累,并参与衰老过程。由于糖尿病和衰老均可导致骨代谢紊乱,甚至出现骨质疏松及脱钙。
AGEs具有广泛的致病作用。AGEs形成后引起蛋白质分子间广泛交联，致使蛋白质结构、机械强度、溶解性和配位结合等性质均发生改变。体内多种蛋白质糖基化可从多个方面影响机体，如引起血管通透性增大、血管基底膜增厚和细胞外基质积聚等。AGEs与其细胞表面受体（RAGE）结合，通过趋化和活化单核巨噬细胞，激活转录因子NF-KB，促进细胞因子和组织因子的释放，灭活一氧化氮和产生氧自由基等途径，参与糖尿病慢性并发症的发生和发展 。由于AGEs的不可逆性，即使高血糖被纠正后，AGEs水平也不能回复到正常，而继续在组织中累积。从组织AGEs自然解释出的反应中间物，如不能经肾脏消除，可再次结合到其他结构上，发生AGEs的“第二次”或“第三次”生成，致病作用加重。