年龄相关性白内障（age-related cataract，ARC）在我国致盲疾病中位居首位，其最主要表现为晶状体变性浑浊，虽其发病机制尚未完全阐明，但氧化应激损伤已被认为是白内障最重要的始发因素。Src-家族酪氨酸激酶（SFK）和血管内皮生长因子（VEGF）在细胞黏着、增殖、迁移、分化和凋亡等过程中都起到重要调控作用，SFK参与了晶状体纤维的分化，且最新研究表明，在无血管存在的晶状体中VEGF一样发挥着重要的作用，SFK/VEGF通路的激活参与了氧化应激致晶状体细胞损伤的过程。在前期临床观察和动物实验基础上，为阐明补青颗粒对大鼠晶状体氧化应激损伤的作用机制，本课题拟分别通过氧化应激诱导器官损伤模型和细胞损伤模型，运用分子生物学、激光共聚焦等先进技术手段，从器官-细胞-分子水平，观察补青颗粒调控SFK-VEGF信号转导通路，干预大鼠晶体状氧化应激损伤的作用及机制。

Age related cataract（ARC）is still a main disease of growing blind in our country,which main presentation is the degeneration of the lens opacity,however,the pathogenesis is not yet clear. Oxidative stress induced by reactive oxygen species has long been implicated in senile cataract formation. It has been known that not only Src-family kinase (SFK) but also Vascular endothelial growth factor (VEGF) played important roles in cell adhesion, proliferation, process migration, differentiation and apoptosis.SFK involved in the differentiation of lens fiber. The latest researches show that it is also vital to the crystalline lens which is absence of blood vessels. Activating SFK/VEGF has take part in the cataract lenses of oxidative damage .Based on the earlier stage of clinical observations and animal experiments, in order to clarify the effects of Buqing granules,our study will observe Buqing granules efficacy by organ model and cell model. Using the molecular biology techniques and confocal laser, we observe the molecular metabolism that Buqing granules whether can regulate SFK/VEGF signaling pathway to prevent the cataract lenses of rats from oxidative stress damage in the organ-cell-molecular level.