慢性肾脏病（CKD）是常见的疑难病，研究如何防治具有重要意义。现已明确，上皮间充质转化（EMT）是CKD发病中的关键环节，且尿外泌体microRNA参与其发生过程。我们前期发现，肾病III号方对CKD有确切疗效，可调节尿外泌体miR-181a-5p的表达异常，经预测EMT关键因子Smad2是它的靶基因。故推测：肾病III号方可能通过调节miR-181a-5p/Smad2延缓肾小管上皮细胞EMT进程，进而治疗CKD。为了验证该假说，本项目拟利用CKD大鼠模型和肾小管上皮细胞EMT模型，围绕尿外泌体miR-181a-5p开展体内外实验研究，以肾病III号方为干预手段，采用基因转染、qPCR、荧光素酶报告基因等技术和方法，明确尿外泌体miR-181a-5p/Smad2在CKD肾小管上皮细胞EMT中的作用，阐明肾病III号方改善肾小管上皮细胞EMT的分子机制，为其临床应用提供依据。

Chronic kidney disease (CKD) is a common and difficult disease, it is of great significance to study how to prevent it. It has been established that epithelial-mesenchymal transition (EMT) is a key link in the pathogenesis of CKD, and that urinary exosomes microRNA is involved in its development. Our previous study found that Shenbing Decoction III has a definite curative effect on CKD and can regulate the abnormal expression of urinary exosomes miR-181a-5p, and it is predicted that Smad2, the key factor of EMT, is its target gene. Therefore, it is speculated that Shenbing Decoction III may delay the progression of EMT in renal tubular epithelial cells by regulating miR-181a-5p/Smad2, and then treat CKD. In order to verify this hypothesis, this project intends to use the CKD rat model and the renal tubular epithelial cell EMT model to conduct in vitro and in vivo experimental studies around the urinary exosomes miR-181a-5p, using Shenbing Decoction III as an intervention method, using techniques and methods for gene transfection, qPCR, luciferase reporter gene to clarify the role of urinary exosomes miR-181a-5p/Smad2 in EMT of CKD renal tubular epithelial cells, and to elucidate the molecular mechanism of Shenbing Decoction III in improving EMT of renal tubular epithelial cells, and provide evidence for its clinical application.