摘要
目的观察卡托普利对左室心肌血管紧张素Ⅱ-1型受体mRNA表达及其受体蛋白的影响,探讨卡托普利逆转左室重构的机制。方法 36只大鼠分为假手术组、模型组和卡托普利组,每组12只。采用RT-PCR方法检测心肌组织AT1mRNA的表达,采用免疫组织化学染色方法观察心肌组织AT1受体蛋白的改变。结果模型组大鼠左心室心肌组织AT1mRNA表达较假手术组升高(P<0.01),卡托普利组左心室心肌组织AT1mRNA表达较模型组显著下降(P<0.01)。模型组大鼠左心室心肌组织AT1受体蛋白较假手术组升高(P<0.01),卡托普利组左心室心肌组织AT1受体蛋白较模型组显著下降(P<0.01)。结论压力负荷所致心肌肥厚大鼠左心室心肌中AT1基因转录与AT1蛋白合成水平是升高的;卡托普利对压力负荷所致心肌肥厚大鼠左心室心肌AT1基因转录与翻译水平均有影响。
Objective To observe the effects of captopril on the expression of left ventricular myocardial type 1 angiotensin Ⅱ （AT1） receptor mRNA and its receptor protein in rats with pressure overload and to investigate the mechanism of regressing left ventricular remodeling. Methods RT-PCR was used to detect the expression of left vcntricular myocardial AT1 receptor mRNA. The change of myocardial AT1 receptor protein were observed by immunohistochemistry. Results The ATt mRNA expression of left ventricular myocardial tissue in model group was significantly higher than that of sham operation group （ P 〈 0.01 ） , which in captopril group was significantly lower than that of model group（ P 〈0.01 ）. The myocardial AT1 receptor protein in model group was obviously higher than that in sham operation group （ P 〈 0.01 ）, which in captopril group was significantly lower than that in model group （ P 〈 0.01 ）. Conclusion The transcription of AT1 receptor gene and synthesis of AT1 receptor protein in left ventricular myocardial tissue are increased in rats with cardiac hypertrophy caused by pressure overload. The transcription and translation of AT1 receptor gene is affected by captopril in rats with the cardiac hypertrophy.
出处
《河北医药》
CAS
2010年第13期1684-1686,共3页
Hebei Medical Journal
基金
南京军区南京总医院科研基金资助项目(编号:Q2008042)
