中文摘要：

目的：本文通过观察血管紧张素Ⅱ（angiotensinⅡ，AngⅡ）影响肾小管上皮细胞转分化（epithelial—mesenchymal transition,EMT）的作用，以及和转化生长因子-β1（transforming growth factor，TGF-β1）作用的关系，探讨AngⅡ参与肾小管间质纤维化的作用机制。方法：以人肾小管上皮细胞株（human kidney cell）HKC细胞为研究对象，采用蛋白印迹等方法，观察AngⅡ（10^-9、10^-8、10^-7、10^-6 mol／L），及其与TGF-β1共同作用对该细胞表达α-平滑肌肌动蛋白（α-smooth muscle actin，α-SMA）、E-钙黏蛋白（E-cadherin）和纤维连接蛋白（fibronectin，FN）的影响。明胶酶谱法检测细胞培养上清液中基质金属蛋白酶-2和基质金属蛋白酶-9（MMP-2和MMP-9）的变化，Boyden小室检测HKC细胞的迁移能力。结果：①单独应用AngⅡ不能够造成HKC细胞E-cadherin表达的变化，也不能诱导α-SMA表达，但是却能上调FN的表达；②与TGF-β1共同作用时能够加强TGF-β1影响E—cadherin，α-SMA和FN表达的作用；③AngⅡ能够增加HKC生成MMP-2和MMP-9；④AngⅡ能够（10^-7和10^-6 mol／L）增加HKC细胞迁移至Boyden小室膜下侧面的数目。结论：①AngⅡ可以参与EMT过程，但不是导致EMT的关键因素；②AngⅡ能够以协同的方式参与TGF-β1导致的EMT，可能以此方式加重肾小管间质的纤维化。

英文摘要：

Objective：To investigate the effect of Angiotensin Ⅱ （Ang Ⅱ ）on renal tubular Epithelial-Mesenchymal transition,evaluate the relationship between Ang Ⅱ and transforming growth factor-β1 （TGF-β1） and discuss the mechanism of Ang Ⅱ involved in tubulointerstitial fibrosis. Methods：Human proximal tubular epithelial HKC cells were taken as research objects. They was maintained in DMEM/F12 medium supplemented with 10% newborn calf serum, α-SMA,E-cadherin and FN triggered by Ang Ⅱ （10^-9, 10^-8, 10^-7,10^-6 mol/L）,and the combination of TGF-β1 were tested by Western blot. The changes of MMP-2 and MMP-9 in supernatant were detected by gelatin zymogramphy. The migration of HKC was assayed by Boyden chamber. Results： （1）In HKC induced by Ang Ⅱ only, the expression of α-SMA and E-cadherin proteins has no change, while FN was highly expressed. （2）α-SMA, E-cadherin and FN triggered by combination of TGF-β1 and Ang Ⅱ was up-regulated,and Ang Ⅱ could enhance the effect of TGF-β1. （3）Ang Ⅱ up-regulated MMP-2 and MMP-9 expressions of HKC. （4）Ang Ⅱ （ 10^-7, 10^-6 mol/L） could increase the number of cells that migrated across the filter and attached to the underside of boyden chamber. Conclusion： （1）Ang Ⅱ was involved in EMT,while it was not the critical factor of EMT. （2）Ang Ⅱ cooperated with TGF-β1 was involved in EMT and might aggravate tubulointerstitial fibrosis.