糖尿病性白内障（Diabetic Cataract，DC）以晶状体混浊为主要特征，是糖尿病晚期的主要并发症，而晶状体的渗透性膨胀是DC早期相对可逆的病理机制，其发病机制尚未完全阐明。最新研究结果显示：“自噬”（Autophagy）与糖尿病的发生发展密切相关，且“线粒体自噬”是晶状体细胞的主要自噬方式。因此，我们认为：“线粒体自噬”相关基因可能成为治疗早中期DC的新靶点。在相关前期研究基础上，为阐明补青颗粒对早中期2型糖尿病小鼠晶状体的影响及作用机制，本课题分别通过器官损伤模型和细胞损伤模型，运用分子生物学、荧光探针、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“线粒体自噬”相关信号转导通路，干预早中期糖尿病小鼠晶体状上皮细胞的作用及机制。

Diabetic cataract (Diabetic Cataract,DC) to lens opacity as the main feature is a major late complication of diabetes,and osmotic swelling of the lens is relatively reversible early pathological mechanism of DC,and its pathogenesis is not fully understood.The latest research results show that:"autophagy"(Autophagy) is closely related to the development of diabetes,and the "mitophagy" is the main way of the lens cells.Therefore,we believe that:" mitophagy" related gene therapy may become a new target for early and mid DC.On the basis of relevant studies,to clarify up BUQING Particles on the lens early and mid type 2 Diabetic mice the effects and mechanisms,through the issue of organ damage model and cell damage model,by using molecular biology,fluorescent probes,laser total focus and other advanced techniques,from organ-cell-molecular level,the regulation was observed up BUQING Particles "mitophagy" related signal transduction pathways,and mechanisms of action to intervene early and mid-crystalline epithelial cells of diabetic mice.