补肾养血明目方基于线粒体途径对视网膜色素上皮细胞氧化应激损伤的保护作用研究

项目名称： 补肾养血明目方基于线粒体途径对视网膜色素上皮细胞氧化应激损伤的保护作用研究

项目编号： No.81503621

项目类型： 青年科学基金项目

立项/批准年度： 2016

项目学科： 医药、卫生

项目作者： 陈强

作者单位： 中国中医科学院眼科医院

项目金额： 18万元

中文摘要： 视网膜色素上皮（RPE）细胞在维持正常眼底结构和视功能方面发挥着不可替代的作用。氧化应激导致的线粒体功能失调及其介导的RPE细胞损伤与年龄相关性黄斑变性（AMD）的发生发展密切相关，其主要的发病机制是活性氧自由基（ROS）导致线粒体膜结构和功能异常及线粒体DNA（mtDNA）损伤所引发的RPE细胞凋亡。因此，减少ROS对线粒体的攻击，稳定线粒体膜结构和膜电位、减少mtDNA的损伤是保护RPE细胞氧化应激损伤的关键途径，亦是防治AMD的重要靶点。补肾养血明目方是名老中医临床多年治疗AMD的经验方，本课题是在前期临床观察和实验研究的基础上，进一步以烟雾中主要化学成分氢醌诱导的小鼠AMD模型及氢醌诱导的体外RPE细胞损伤模型为研究载体，采用细胞分子生物学、病理学、电镜、眼电生理学等研究技术，深入探讨补肾活血明目方对RPE细胞氧化损伤的保护作用及作用机制，为临床治疗AMD提供科学依据。

中文关键词： 补肾养血明目方；视网膜色素上皮细胞；线粒体；氧化应激

英文摘要： Retinal pigment epithelium plays important roles in maintaining the normal retinal structure and visual function. Mitochondrial dysfunction caused by oxidative stress and mediated RPE cell damage has close relationship with the development of age-related macular degeneration, the main pathogenesis is due to RPE apoptosis induced by structure and function anomalies of mitochondrial membrane and mitochondrial damage caused by reactive oxide species. Therefore, reducing the attack of ROS to mitochondrion, stabilizing membrane structure and potential of mitochondrion, decreasing mtDNA damage are the key ways to protect RPE from oxidative stress damage, and also the important targets for AMD prevention. Bu Shen Yang Xue Ming Mu Formula is an empirical formula commonly used in our clinics. This project is designed based on the primary clinical observation and experimental study. With the AMD mouse model induced by cigarette smoke-related Hydroquinone and in vitro RPE damage model induced by Hydroquinone as study objects, by means of modern research techniques like cellular and molecular microbiology approaches, pathology, electron microscopy, ocular electrophysiology, to thoroughly investigate the effect and its mechanism of Bu Shen Yang Xue Ming Mu Fang on protecting RPE from oxidative damage, thus to supply reliable and scientific evidence for clinical application.

英文关键词： Bu Shen Yang Xue Ming Mu Formula;Retinal pigment epithelial cells;Mitochondria;Oxidative stress