目的:观察血管紧张素-(1-7)[Ang-(1-7)]对血管紧张素Ⅱ(AngⅡ)诱导的大鼠肾间质成纤维细胞活化及细胞外基质分泌的影响并初步探讨其机制.方法:体外培养正常大鼠肾间质成纤维细胞(NRK-49F),分为对照组和Ang-(1-7)组、AngⅡ组和Ang-(1-7)+AngⅡ组,培养72 h后,细胞免疫化学染色法检测细胞活化标志物α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1(TGF-β1)和胰岛素样生长因子I(IGF-I)表达;酶联免疫吸附实验(ELISA)检测上清液中TGF-β1、IGF-I及细胞外基质成分Ⅰ型胶原(ColⅠ)的含量.结果:对照组仅有基础水平的α-SMA表达,几无Col I、TGF-β1和IGF-I表达,Ang-(1-7)组与之类似;AngⅡ组细胞α-SMA及ColⅠ、TGF-β1、IGF-I表达较对照组显著增加(P<0.05);AngⅡ+Ang-(1-7)组与AngⅡ组比较,细胞α-SMA及Col I、TGF-β1、IGF-I表达明显减少(P<0.05).结论:Ang-(1-7)可抑制AngⅡ诱导的肾间质成纤维细胞活化,减少细胞外基质成分ColⅠ的合成,其机制可能是通过下调致纤维化细胞因子TGF-β1和IGF-I的表达.%AIM:To explore the influence of angiotensin - (1 -7) [ Ang - (1 -7) ] on angiotension II( Ang II) - induced activation and extracellular matrix secretion in rat renal interstitial fibroblasts( NRK - 49F cells). METHODS: The NRK-49F cells were maintained and sub -cultured, then the cells were divided into control group, Ang II group, Ang - (1 - 7 ) group and Ang II + Ang - (1 - 7) group. The expression of a - smooth muscle actin (a - SMA ) , transforming growth factor Pi (TGF - P, ) and insulin - like growth factor I( IGF -1) was detected by the method of immunocytochemistry when the cells were cultured for 72 h. The content of TGF - β1, IGF -1 and collagen type I( Col I) in the cultured supernatants were measured by ELISA. RESULTS; In control group and Ang - ( 1 -7) group, only basic expression of a - SMA and almost no expression of TGF - β1, IGF -1 and Col I were observed. Compared with control group, the expression of a - SMA, TGF - β1, IGF -1 and Col I was increased in Ang II group. Compared with Ang II group, the expression of o - SMA, TGF - β1, IGF - I and Col I was significantly decreased in Ang II + Ang - (1 - 7 ) group. CONCLUSION : Ang - ( 1-7 ) inhibits the activation of renal interstitial fibroblasts and decreases the Ang II induced secretion of Col I by suppressing TGF - p, and IGF -1 expression.
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