microRNA21通过调节CTGF参与TGF-β1诱导肾间质纤维化的机制及中药扶肾方作用的研究

肾间质纤维化是各种不同病因的慢性肾病进展到ESRD的最终共同病变过程，肾小管上皮－间充质转分化（EMT）是肾间质纤维化的关键致病机理。目前肾小管 EMT 的调控机制仍不十分明确。近来微小核糖核酸 (miRNA)在 EMT 中的作用备受国内外关注。本实验在前期实验基础上，借助RT-PCR、westernblot、基因转染等技术，研究单侧输尿管梗阻大鼠病变侧肾脏组织中miRNA-21、CTGF 的差异表达，在体外实验中观察 miR-21 在TGF-β1诱导的 NRK-52E细胞转分化中的作用，探讨micRNA-21通过调节CTGF参与TGF-β1诱导的肾小管上皮细胞EMT的可能机制，阐明 miR-21 参与调控肾小管EMT 的可能的靶点以及中药扶肾方延缓肾间质纤维化作用机制。

Renal interstitial fibrosis is a chronic kidney disease progress of various etiological factors to the final common process of ESRD, renal tubular epithelial to mesenchymal transition (EMT) is the key pathogenesis of renal interstitial fibrosis. Current renal tubular EMT regulation mechanism is still not clear. Recently, the micro ribonucleic acid (miRNA) on the role of EMT in much attention at home and abroad. The experiments in the previous experimental basis, with the help of RT-PCR, Westernblot, gene transfection technique, differences of expression in unilateral ureteral obstruction rats kidney tissue lesion side in miRNA-21, CTGF,observe the transdifferentiation of miR-21 effect in the TGF- beta 1 induced NRK-52E cells in vitro, and to investigate the possible mechanism by adjusting the CTGF involved in TGF- beta 1 induced renal tubular epithelial cells in EMT micRNA-21, a possible target to elucidate the miR-21 involved in the regulation of renal tubular EMT and renal side of renal interstitial fibrosis mechanism.