摘要
目的探讨卡托普利对腹主动脉缩窄大鼠左室心肌血管紧张素Ⅱ-1型(AT1)受体mRNA表达及其受体蛋白改变的干预作用。方法银夹法建立腹主动脉缩窄大鼠模型,用免疫组化法进行心肌AT1受体蛋白染色,即时PCR扩增后分析并测定其mRNA表达,观察卡托普利对大鼠左室心肌质量指数(LVMl)、病理形态苏木精-伊红染色和心肌AT1受体蛋白与其mRNA表达改变的干预作用。结果造模8周时左室心肌质量指数、左室AT1受体蛋白及其mRNA表达模型组较假手术组显著升高(P<0.01),卡托普利组较模型组显著降低(P<0.01)。结论腹主动脉缩窄大鼠所致心肌纤维化心肌AT1基因转录与翻译水平发生改变,通过AT1下游信号通路传导作用,促进心肌纤维化;卡托普利可延缓甚至逆转心肌的纤维化进程。
Objective To investigate the effects of captopril on left ventricular myocardium angiotensin Ⅱ type-1 receptor and its mRNA expression in abdominal aortic banding model rats.Methods We established abdominal aortic banding rats model with silver clip.Gray scale value of Left ventricular myocardium angiotensin Ⅱ type-1 receptor was measured after immunohistochemistry stain.We determined the exepression of angiotensin Ⅱ type receptor mRNA after real-time PCR amplification and observed the effacts of captopril.Results In the 8th week,LVMI,average optical density value and the mRNA expression of left ventricular myocardium angiotensin Ⅱ type-1 receptor were incressed obviously in model group,compared whit sham-operation group（P〈0.01） and comparing to model group,these index were decreased in captopril group.Conclusion This study supports that the level of AT1 transcription and translation increase in model rat with myocardial fibrosis established by partially abdominal aorta banding,which enhance the signaling path of Ang Ⅱ-AT1 and contribute to myocardial fibrosis;captopril may delay even regress the process of myocardial fibrosis.
出处
《四川医学》
CAS
2010年第8期1044-1047,共4页
Sichuan Medical Journal
基金
江苏省"六大人才高峰"资助基金(编号:2005A2)
