基于回医“四性学说”研究回回甘松饮调控miR-192保护糖尿病肾病大鼠的作用及分子机制

项目名称： 基于回医“四性学说”研究回回甘松饮调控miR-192保护糖尿病肾病大鼠的作用及分子机制

项目编号： No.81202774

项目类型： 青年科学基金项目

立项/批准年度： 2013

项目学科： 医学八处

项目作者： 袁玲

作者单位： 宁夏医科大学

项目金额： 23万元

中文摘要： 糖尿病肾病（DN）是严重危害人类健康的疾病,但其机制尚未彻底阐明。miR-192是唯一被发现在肾小球系膜细胞表达的miRNA,其直接靶基因SIP1是TGF-β1/Smad通路的重要节点。我们推测：miR-192与靶基因结合可有效调控TGF-β1/Smad信号通路,这可能是DN发病的一个新机制。针对宁夏回族DN发生率高的现状，前期研究发现：基于回医"四性学说"组方的回回甘松饮（HGY）有效改善宁夏回族DN患者症状；并可降低糖尿病动物模型的血糖与血脂。在此基础上，为阐明HGY对DN的药效及分子机制，本课题拟通过大鼠DN模型，观察HGY药效，并运用分子生物学等技术通过在体和离体实验观察HGY是否以miR-192为靶点，调控TGF-β1/Smad信号通路,参与细胞外基质(ECM)代谢。本课题从回族医学理论出发，以miR-192为切入点，阐明HGY对DN的药效及机制，为防治DN提供新思路和新靶点。

中文关键词： 回回甘松饮；细胞外基质；microRNA-192；TGF-β1/Smads信号通路；

英文摘要： Diabetic nephropathy has become one of the major diseases which threaten the Public health . The mechanism of DN has not been elucidated thoroughly yet. MiR-192 is the only miRNA which has been found in glomerular mesangial cells. Its direct target genes is SIP1 which is the important node of TGF-β1/Smad pathway . We hypothesized that: miR-192 may bind to SIP1 which can effectively control TGF-β1/Smad signal pathway, and it may be a new mechanism of DN . It was found in previous research that Hui-hui Gan-song Yin ( HGY )which is based on the "FOUR XING Theory" is effective in improving symptoms of DN patients of Hui nationality in Ningxia. And it can also reduce the level of blood glucose and blood lipid in diabetic animal model. On this basis, in order to clarify the effects of HGY on DN and its molecular mechanism, our study will observe HGY efficacy by rat DN model. Using the Molecular Biology techniques and Flow cytometry, we observe whether HGY regulates TGF-β1/Smad signaling pathway by the target point of miR-192 or involves in extracellular matrix (ECM) metabolism in the whole - cell-molecular level. This study based on the Hui nationality medicine theory, miR-192 as the starting point, elucidates the efficacy of HGY and the mechanism, providing a new thought and new target on the prevention of DN.

英文关键词： Huihui Gansong Yin；extracellular matrix；microRNA-192；TGF-β1/Smads signal pathway；