晚期糖基化终末产物与糖尿病神经病变

非酶糖基化反应是糖尿病神经病变的重要发病机制之一。持久高血糖使体内晚期糖基化终末产物（AGEs）不断积累，沉积于神经组织的AGEs不仅修饰了细胞骨架蛋白、髓鞘蛋白及基质蛋白等，从而直接损害神经结构与功能，而且还通过增强氧化应激反应，或与神经元表面AGEs受体（RAGE）作用进一步导致神经功能紊乱。AGEs还可引起神经微循环障碍。单用或联用AGEs抑制剂、抗氧化剂、可溶性RAGE及抗RAGE IgG在防止、缓解、逆转糖尿病神经病变中显示出巨大的潜力。

The relationship between advanced glycation end-products and diabetic neuropathy

Non-enzymatic glycation is implicated in the pathogenesis of diabetic neuropathy(DN).Long term hyperglycaemic condition leads to increased formation and accumulation of advanced glycation end-products(AGEs) in nerve tissue.AGEs modified structural protein such as cytoskeletal protein,myelin protein and matrix protein.And that may result in functional and structural abnormalities of nerve fibers.AGEs also may enhance oxidative stress,interact with receptor for AGEs(RAGE) binding on neuron and alter the endoneurial microcirculation,thereby contributes to the development of DN.AGEs inhibitors,soluble RAGE and anti-RAGE IgG have shown great promise in the prevention,delay and reversal of DN.