糖尿病肾病(DN)是糖尿病的严重并发症之一。研究表明miRNA-155通过抑制或降解靶基因mRNA参与生物体的多种生理及病理过程，尤其在糖尿病肾病的发生及进展起到重要作用，但是miRNA-155具体调节哪些基因参与DN的分子机制尚不清楚。前期基础研究表明，miR-155与IRS-1基因有共同的结合位点，同时，知母皂苷BII能够显著改善DN的症状，并通过IRS-1/PI3K/Akt通路减轻糖尿病的胰岛素抵抗。知母皂苷BII是否能够通过miR-155调控的IRS-1/PI3K/Akt轴改善DN症状是本项目研究的重点。本项目拟采用足细胞损伤模型和STZ诱导的DN动物模型，结合免疫组织化学、RT-PCR等技术方法，从细胞、整体，以及分子水平综合评价知母皂苷BII对miR-155调控的IRS-1/PI3K/Akt轴相关指标的影响，阐明知母皂苷BII防治DN的作用机制，以期为中药抗DN提供新思路。

Diabetic nephropathy (DN) is a serious complication of diabetes. Studies have shown that miR-155 is associated with the development and progression of diabetic nephropathy. The mechanism may be through regulation of IRS-1, PI3K and Akt levels, but it is unclear whether exosome miR-155 is involved in this process. Our previous studies showed that timosaponin BII can ameliorate the symptoms of diabetic nephropathy through the IRS-1/PI3K/Akt pathway. Based on the preliminary work, this project intends to use the model of podocyte injury to explore the effect of timosaponin BII on the expression levels of miR-155, IRS-1, PI3K and Akt, and to use a single high-dose intraperitoneal injection. Streptozotocin (STZ) was used to construct an animal model of DN to verify that timosaponin BII improved DN through the IRS-1/PI3K/Akt axis regulated by exosome miR-155, in order to provide new ideas for anti-diabetic nephropathy of traditional Chinese medicine.