摘要
目的 :观察血管紧张素 ( 1 7) [Ang ( 1 7) ]对实验性肾性高血压大鼠肾组织纤维化的影响。方法 :采用微渗泵植入技术 ,建立Ang ( 1 7)对二肾一夹 ( 2K1C)高血压大鼠干预模型 ,在光镜下观察肾脏纤维化 ,免疫组化法检测肾组织转化生长因子β1 (TGF β1 ) ,RT PCR检测肾组织内TGF β1 、TGF β1 受体ImRNA水平。结果 :Ang ( 1 7)能减轻2K1C高血压大鼠肾纤维化 ,减少 2K1C高血压大鼠肾组织TGF β1 的蛋白表达 ,降低肾组织内TGF β1 、TGF β1 受体ImRNA水平。结论 :Ang ( 1 7)对 2K1C高血压大鼠肾纤维化作用机制之一是通过减少肾组织内TGF β1
Objective: To investigate the effects of Angiotensin-(1-7) on renal fi-brosis in renal vascular hypertension in rats.Method: 2-kidney 1-clip(2K1C) hypertensive rat model was established, and the technique of micro-osmotic pump was used to establish the Ang-(1-7) intervention hypertensive rat model, Renal fibrosis changes were observed by light microscope, Changes of transforming growth facterβ 1(TGF-β 1) in renal were observed by immunohistochemistry, TGF-β 1 and TGF-β receptor I mRNA in renal was measured by RT-PCR.Results: After Ang-(1-7) intervention, renal fibrosis induced by hypertension were significantly reduced. Levels of TGF-β 1 in renal were significantly reduced. The expression of TGF-β 1 and TGF-β receptor I mRNA in renal was significantly down-regulated.Conclusion: Ang-(1-7) can reduce renal fibrosis induced by hypertension in 2K1C hypertensive rats,TGF-β 1 and TGF-β receptor I play an important role in this process.
出处
《微循环学杂志》
2004年第2期21-23,26,F003,共5页
Chinese Journal of Microcirculation
