文档介绍：κ阿片受体激动对血管紧张素Ⅱ诱导心肌肥大的抑制作用
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作者:张伟,王洪新,吴国强,刘杰
【摘要】目的通过观察κ阿片受体激动对血管紧张素II诱导心肌肥大的作用,研究κ阿片受体激动剂对血管紧张素II诱导心肌肥大的抑制作用。方法以体外培养的乳大鼠心肌细胞为模型,应用血管紧张素II1 μM诱导心肌肥大,观察U50488H1 μM对它的作用,并和洛沙坦(los)1 μM组做对比观察κ阿片受体的激活对心肌肥大的作用。用Lowry法检测心肌细胞蛋白含量;用消化分离法及计算机图像分析系统检测心肌细胞体积;用[3H]-leueine掺入法测定心肌细胞蛋白的合成。结果 AngII1 μM使心肌细胞总蛋白含量,蛋白表达及细胞体积明显增加;U50488H1 μM能够降低由AngII引起的心肌细胞蛋白含量,蛋白表达,以及体积的增加,从而抑制心肌肥大,并且抑制程度与los1 μM相似。结论κ阿片受体激动剂U50488H能够抑制由AngII诱导的心肌细胞肥大。
【关键词】心肌肥大κ阿片受体 U50488H 血管紧张素II
Abstract: Objective To demonstrate the inhibitory effect of
κ-Opioid on AngII-induced hypertrophy in cultured myocardial cells of neonatal rats. Methods Based on the model of cardiac bistiocyte cells in vitro culture, the experiment applies the angiotensin II1 μM to induce the myocardium to be hypertrophy. Compared with the group of (los) 1 μM, the experiment observes the effects of the activation of κ-Opioid on myocardial hypertrophy. The protein content was measured by Lowrys method. The protein synthetic rate was obtained through measuring the incorporation of [3H]-leueine into myocyte protein by liquid scintillation method,the cardiomyocytes volumes were measured puter photograph analysis system; the pound of the cardiac bistiocytes was measured by the incorporation method of [3H]-leueine. Results AngII (1 μM) can increase the overall protein content, proteinemia expression, and the cells volumes. U50488H1 μM can reduce the protein content of cardiac bistiocyte, protein expression and the cells volumes, which are induced by AngII. Therefore, U50488H1 μM inhibits the myocardial hypertrophy and it has the similar inhibitive extent with the los1 μM. Conclusions κ-Opioid receptor stimulation U50488H can inhibit hypertrophy induced by AngII in neonatal rat ventricular myocytes.
Key words:myocardial hypertrophy;
κ-Opioid; U50488H; Angiotersin II
心肌组织上存在κ阿片受体(κ-OR)[1],近年来关于κ-OR对心肌细胞生长和肥厚的研究较多,本实验室的研究也已经证实κ-OR是心肌细胞的负性调节因子[2]可以抑制去甲肾上腺素诱导的心肌肥大[3], 并表明选择性κ-OR激动