糖尿病心肌病（DCM）发病率高，危害大，纤维化是DCM核心病理改变，目前无有效防治药，而内皮-间质转换（EndMT）是心肌纤维化的重要机制。研究发现RAS系统激活后AngⅡ可下调miR-133a、活化TGF-β/Smad通路而加剧心肌纤维化。益消方是课题组研发治疗DCM有效方剂，并发现其可抑制RAS的激活，使AngⅡ表达减少，抑制心肌重构进程，但益消方是否通过上调miR-133a表达，抑制TGF-β/Smads-snail/CTGF信号通路的激活，减轻EndMT，干预DCM心肌纤维化尚未见报道。本课题拟采用激光共聚焦、RNA seq及流式细胞等分子生物学技术，从miR-133a调控TGF-β/Smads-snail/CTGF通路介导EndMT角度，研究益消方干预DCM小鼠的分子机制，并用人心肌成纤维细胞验证，以期发现其可能的作用靶点和调控机制，对探讨中药作用机制及新药研发具有重要意义。

Diabetic cardiomyopathy (DCM)is characterized by high incidence and great harm.Fibrosis is the core pathological change of DCM,but there is no specific chemical medicines for DCM yet currently.Endothelial-mesenchymal transition(EndMT) has been considered as an important mechanism of myocardial fibrosis in DCM.The current study found that RAS system increased AngII levels,down-regulated the expression of miR-133a,activated TGF-β/ Smad pathway and aggravated myocardial fibrosis.Yixiao Decoction is an effective chinese herbal compound prescription of clinical treatment of DCM for many years. In previous research we found that Yixiao Decoction can inhibit the activation of RAS,resulting in down-regulation of AngⅡ and reducing cardiac remodeling process.But there haven't been reported that whether Yixiao Decoction can inhibit the activation of TGF-β/ Smads-snail / CTGF signaling pathway , alleviate EndMT by up-regulating the expression of miR-133a to treat myocardial fibrosis of DCM .We intend to study the molecular mechanism of Yixiao Decoction’s intervention in DCM mice and validate it with human cardiac fibroblasts from the perspective of miR-133a in the regulation of EndMT mediated by TGF-β/ smads-snail / CTGF pathway by using laser confocal, RNA seq, flow cytometry and other technologies in this research.The research aims to find out the potential possible target and regulatory mechanism of Yixiao Decoction in treating DCM,it will have great significance to explore the mechanism of chinese medicine and the development of new drug research.