血管紧张素Ⅱ参与肾间质成纤维细胞自分泌TGF- β1 的实验研究

Effects ofAngiotensin Ⅱ on Autocrine Secretion of TGF- β1 by Renal Interstitial Fibroblast

目的通过观察血管紧张素Ⅱ（AngiotensinⅡ，AngⅡ）对正常大鼠肾间质成纤维细胞株NRK．49F自分泌TGF- β1 的影响，探讨其参与肾小管间质纤维化的作用机制。方法用不同浓度Ang1I（10^-6,10^-7,10^-8, 10^-9mol／L）刺激NRK．49F（6h，12h，24h，和48h）。蛋白免疫印迹法检测TGF- β1 受体（T13RD的表达。ELISA方法检测细胞上清液中TGF-1的浓度。结果（1）AngⅡ（10^-7mol／L）能刺激NRK-49F细胞分泌TGF- β1 ，其表达量在刺激细胞6h后即开始增加，12h后达到峰值，24h和48h仍能维持较高的水平；（2）AngⅡ（10-9mol／L）能够上调NRK．49F细胞TBRI的表达。结论AngⅡ参与肾问质成纤维细胞自分泌TGF- β1 ，从而促进。肾小管问质纤维化的发生发展。

Objective To further investigate the mechanism of Angiotensin Ⅱ on interstitial fibrosis,the effects of Angiotensin Ⅱ on autocrine secretion of TGF-β1 by rat renal interstitial fibroblast（NRK-49F） were explored. Methods Different concentrations of Angiotensin Ⅱ （10^-6,10^-7,10^-8, 10^-9）mol/L stimulating normal rat renal intersti- tial fibroblast （NRK-49F） were cultured for 6h, 12h, 24h and 48h.Western Blot detected TGF βRI（T βRI）. ELISA detected TGF-β1in the supernatant ofNRK-49F.Results （1）Ang II stimulated secretion of TGF-β1 as early as 6h after Ang Ⅱ were induced and lasted until 48h.（2）Ang Ⅱupregulated T β RI expression. Conclusion Ang 1I can stimulate autocrine secretion of TGF- β1 by rat renal interstitial fibroblast, which suggested that the effects ofAng Ⅱ on fibroblast might associate with the development of CKD.