肾小管上皮间质转分化（EMT）是糖尿病肾病（DN）肾间质纤维化早期事件。芪葵颗粒能抑制肾小管EMT，但分子机制不明。RNA之间相互作用是调控肾小管EMT的重要机制。前期研究表明，TUG1是芪葵颗粒干预DN小鼠后肾组织高表达的LncRNA。TUG1与miR-377有结合位点，PPARγ是miR-377的靶基因。芪葵颗粒能上调TUG1和PPARγ，下调miR-377表达。我们推测，芪葵颗粒可能通过TUG1/miR-377途径调控肾小管EMT，发挥抗DN肾间质纤维化的作用。本课题拟进行：高糖诱导肾小管EMT，采用沉默、过表达、双荧光素酶报告基因等技术，验证TUG1竞争性结合miR-377，上调PPARγ，抑制肾小管EMT。进一步证实芪葵颗粒通过TUG1/miR-377途径抑制肾小管EMT。采用db/db小鼠DN模型，明确芪葵颗粒抑制肾间质纤维化的效应环节及作用靶点，为中医药防治DN提供科学依据。

Renal tubular epithelial mesenchymal transition (EMT) is an early event of renal interstitial fibrosis in diabetic nephropathy (DN). Qikui granules can inhibit renal tubular EMT, but the mechanism is unknown. The interaction between RNAs is an important mechanism for regulation of renal tubular EMT. Previous studies showed that TUG1 is a highly expressed lncRNA in kidney tissue of DN mice after intervention of Qikui granules; there are binding sites between TUG1 and miR-377; PPARγ is the target gene of miR-377; Qikui granules can up-regulate the expression of TUG1 and PPARγ and down-regulate the expression of miR-377. We speculate that Qikui granules may regulate renal tubular EMT through TUG1/miR-377 pathway, and inhibit renal interstitial fibrosis. In this subject, we induce renal tubular EMT by high glucose, use technologies of silence/overexpression, double luciferase reporter gene and et al to verify the competitive binding of TUG1 to miR-377, up-regulate PPARγ, inhibit renal tubular EMT. We confirm that Qikui granules inhibit renal tubular EMT through TUG1/miR-377/PPARγ. Using the db/db mouse DN model, we verify the effective link and target of Qikui granules in inhibiting renal interstitial fibrosis, which provides scientific basis for prevention and treatment of DN by traditional Chinese medicine.