视网膜色素上皮细胞光氧化损伤及原花青素B2的保护作用

Photooxidation-induced damage in retinal pigment epithelium and protective effect of procyanidins B2

蓝光可诱导视网膜色素上皮(RPE)细胞发生光损伤,是年龄相关性眼病的主要发病机制之一。随着年龄增长,脂褐素在RPE细胞中沉积,蓝光能诱导RPE细胞中的脂褐素产生活性氧自由基(ROS),导致光氧化损伤。为了进一步研究蓝光诱导RPE细胞损伤的机制,采用累积了脂褐素主要成分N-亚视-N-视黄基-乙醇胺(A2E)的ARPE-19细胞作为RPE细胞光氧化损伤模型,对细胞活性、ROS、内质网应激(ER stress)蛋白及caspases进行检测,结果显示蓝光可降低RPE细胞活性,增加了ROS生成量,并且与内质网应激(ER stress)反应以及caspase-9和caspase-3的活化相关。此外,经原花青素B2处理后,RPE细胞活性显著提高,并且过氧化物歧化酶(SOD)活力及还原型谷胱甘肽(GSH)含量显著增加。这些结果表明,葡萄原花青素B2可能通过提高细胞内抗氧化酶活力降低氧化应激反应,从而抑制蓝光诱导RPE细胞损伤。

Blue light may induce photodamage in retinal pigment epithelium （RPE）, which is one of the major mechanism of age related eye diseases. Lipofuscin gradually accumulates in RPE cells with age. Blue light induces lipofuscin to produce active oxygen radicals （ROS）,which causes photooxidative damage in RPE cells. To further demonstrate the mechanism by which blue light induces photodamage in RPE cells, ARPE-19 cells accumulated with A2E, one of the lipofuscin fluorophores, were used as a model system, and cell viability, ROS, edoplasmic reticulum （ER） stress markers and caspases were detected. The results showed that blue light reduced cell viability and increased ROS production, which is associated with ER stress and the activation of caspase-9 and caspase-3. In addition, pretreatment with procyanidins B2 （PB2） significantly improved cell viability,increased superoxide dismutase （SOD） activity and glutathione （GSH） production. Taken together, these results suggested that PB2 inhibited blue light-induced photodamage in RPE cells via promoting antioxidase activity and reduced oxidative stress.