研究发现心脏自身拥有一组心肌多潜能干细胞，可以分化为心肌细胞以维持心肌自我更新与修复；持续的高血糖诱导心肌多潜能干细胞的氧化应激损伤是糖尿病心肌病的重要发病机制。我们前期研究结果显示黄芪多糖对糖尿病心肌病有明确的保护作用。进一步研究我们发现，黄芪多糖治疗后，糖尿病鼠心脏的心肌多潜能干细胞含量增加、氧化应激产物减少、SOD2(线粒体过氧化物歧化酶）蛋白表达增高；黄芪多糖干预后，高糖培养下小鼠心肌多潜能干细胞的凋亡减少、氧化应激产物减少、SOD2蛋白表达增高；提示黄芪多糖对糖尿病心肌病的保护作用与心肌多潜能干细胞的氧化应激损伤密切相关，然而其机制尚不清楚。本课题将以小鼠心肌多潜能干细胞培养、部分敲除SOD2基因的转基因小鼠为模型，在动物水平和细胞水平深入探讨黄芪多糖通过调控SOD2表达对糖尿病心肌多潜能干细胞氧化应激损伤的阻断机制，为黄芪多糖治疗糖尿病心肌病提供进一步的理论依据和实验基础。

Accumulating evidence supports that the heart possesses a compartment of multipotent stem/ progenitor cells (CSPCs) that differentiate into cardiomyocytes to renew itself. Enhanced CSPCs apoptosis mediated by oxidative stress may result from hyperglycemia in diabetic cardiomyopathy. Our previous study showed that Astragalus Polysaccharides (APS) treatment prevented myocardial ultrastructure abnormality and cardiac dysfunction in diabetic mice. Moreover, APS treatment led to less ROS production, less CSPCs apoptosis and upper-expression of SOD2 protein both in CSPCs cultured with hyperglycemia and in hearts of diabetic mice. However, the exact effect of APS on oxidative stress-dependent apoptosis of CSPCs in diabetic cardiomyopathy is still unkown. Therefore, in the present study, we will use CSPCs culture and SOD2 KO mice to explore the role of APS in oxidative stress-dependent apoptosis of CSPCs in diabetic cardiomyopathy, and the relevant mechanism involving redox signaling pathway and SOD2 protein regulation. This project may provide further rationale and more evidence for the APS treatment on diabetic cardiomyopathy.