核因子-κB在糖尿病视网膜病发病机制中的研究进展

Nuclear factor kappa B and diabetic retinopathy

糖尿病视网膜病是糖尿病的严重并发症。糖尿病视网膜中核因子-κB(NF-κB)能被糖尿病所致的氧化应激等活化,NF-κB的异常活化能增加细胞因子,细胞间黏附分子-1等的表达,从而参与糖尿病视网膜病的发生、发展。NF-κB活化可导致视网膜周边细胞凋亡、白细胞黏附到血管内皮上、毛细血管基膜增厚、新生血管形成,并且参与视网膜前膜的形成。NF-κB在糖尿病视网膜病的发病机制中发挥着重要作用。因此,抑制NF-κB的活化以防治视网膜病已成为糖尿病视网膜病治疗的一个新策略。作者就近年来NF-κB在糖尿病视网膜病中的研究进展作一综述。

Diabetic retinopathy is a highly specific vascular complication of both type 1 and type 2 diabetes. NF-κB can be triggered by oxidative stress and controls several programs of gene expression, the majority of which participate in the host inflammation and immune response. Evidence has accumulated that NF-κB is involved in the development of diabetic retinopathy. NF-κB activation induced by diabetes is associated with the apoptosis found in the pericyte, leukocyte-endothelial interaction, capillary basement membrane thickening, neovascularization and formation of epiretinal membranes. Inhibition of NF-κB activation has been suggested as a treatment strategy in diabetic retinopathy.