作者: Jinyun Pu , Yu Zhang , Jianhua Zhou
DOI: 10.1155/2016/8612190
关键词: Renal Tubular Epithelial Cells 、 Cancer research 、 Pathology 、 Repressor 、 Epithelial–mesenchymal transition 、 Renal fibrosis 、 In vitro 、 Kidney 、 Fibrosis 、 In vivo 、 Medicine
摘要: Epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells is a vital mechanism fibrosis. Mounting evidence suggests that miR-200a expression decreases in unilateral ureteral obstruction (UUO) rats. Moreover, it has been demonstrated Huai Qi Huang (HQH) can ameliorate tubulointerstitial damage adriamycin nephrosis and delay kidney dysfunction primary glomerular disease. However, the effect HQH on EMT UUO rats its molecular unclear. In order to explore fibrosis, vitro vivo experiments were performed our study. Our results showed increased TGF-β1 stimulated NRK-52E cells. Meanwhile, decreased ZEB1 ZEB2 (the transcriptional repressors E-cadherin), α-SMA vivo. Furthermore, we found protected from fibrosis The regulated miR-200a/ZEBs pathway inhibited process, which may be protecting