蛋白激酶C-β及其抑制剂与糖尿病视网膜病变

PKC-β, its inhibitor and diabetic retinopathy

糖尿病视网膜病变的生化机制之一是高糖诱导的蛋白激酶C-β活化导致细胞信号的改变。经典的蛋白激酶C-β活化主要是二酰基甘油释放增加及多种致炎细胞因子参与的结果。近年的实验室研究及临床研究报道显示，ruboxistaurin是一种蛋白激酶C-β抑制剂，可预防糖尿病视网膜病变及糖尿病黄斑水肿的进展。本文就蛋白激酶C-β与糖尿病视网膜病变的发生及其抑制剂ruboxistaurin对糖尿病视网膜病变的治疗机制、疗效、安全性及前景进行综述。

One of the biochemical mechanism of diabetic retinopathy （DR） is the activation of protein kinase C-β（PKC-β） induced by high level glucose,which leads to cellular signal changing. PKC-β is activated mainly through the release of diacylglycerol and with multiple proinflammatory cytokines participation. Recently ,laboratory and clinical researches demonstrate that ruboxistaurin （LY333531） , an inhibitor of PKC-β, can slow down the development of DR and macular edema. This article focuses on the therapeutic mechanism of PKC-β inhibitor of DR, and its therapeutic effect, safety and prospect.