炎症在糖尿病视网膜病变发病机制中的作用

The role of inflammation in diabetic retinopathy

糖尿病视网膜病变(DR)是糖尿病常见的严重并发症,也是主要的致盲疾病之一,其发病机制尚不清楚。近年的研究发现早期糖尿病视网膜中白细胞粘附增加,并与DR微血管损伤在时间和空间上一致。同时细胞内粘附分子-1(ICAM-1)及其基因表达上调,抗ICAM-1抗体及CD18抗体可抑制糖尿病引起的白细胞粘附和血管内皮损伤。血管内皮生长因子(VEGF)和糖基化终产物(AGEs)可引起DR中的炎症改变。增加视网膜内VEGF及AGEs可明显增加白细胞粘附和血-视网膜屏障的破坏。非甾体类抗炎药物可能参与抑制糖尿病视网膜炎症。

Diabetic retinopathy （DR）, a common severe complication of diabetes, is one of the leading causes of blindness. The mechanisms underlying DR remain largely unknown. The current studies demonstrate that adherent leukocytes （leukostasis） in retina increase at early stage of DR, which are temporally and spatially associated with diabetic retinal microvascular injury. The expression of intracellular adhesion molecule-1 （ICAM-1）and genes encoding neutrophil adhesion proteins are enhanced during the same period of DR. Moreover, it the antibody-based neutralization of ICAM-1 and CD18 is shown that prevent both leukocyte adhesion and retinal endothelial cell injury induced by diabetes. Vascular endothelial growth factor （VEGF） and advanced glycation end products （AGEs） can induce the inflammatory component of the DR. The increase of VEGF and AGEs in the retina could induce leukostasis and breakdown of blood-retinal barrier. Nonsteroidal anti-inflammatory drugs may contribute to preventing the inflammation component of DR.