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目的:在原代培养的新生大鼠心肌细胞上观察辛伐他汀对血管紧张素Ⅱ(AngⅡ)及心肌营养素-1(CT-1)致心肌细胞肥大的防治作用。方法:应用改进的Simpson方法进行原代SD大鼠心肌细胞培养,制备全细胞提取液;通过改良Lowry法测定心肌细胞总蛋白含量;采用相差显微镜和HJ2000通用图像分析系统测定心肌细胞表面积,并为卡托普利作阳性对照。结果:①剂量为10-6mol/L的辛伐他汀能安全有效地抑制AngⅡ诱导的心肌细胞总蛋白含量的增加和心肌细胞表面积的增大,其效果与血管紧张素转化酶抑制——卡托普利作用相似。②CT-1呈剂量依赖性诱导心肌细胞总蛋白含量增加;辛伐他汀能明显抑制CT-1诱导的心肌细胞总蛋白含量的增加和心肌细胞表面积的增大。结论:辛伐他汀能明显抑制AngⅡ及CT-1诱导的心肌细胞总蛋白含量的增加和心肌细胞表面积的增大,具有防治心肌细胞肥大的作用。
OBJECTIVE: To observe the preventive and therapeutic effect of simvastatin on cardiomyocyte hypertrophy induced by angiotensin Ⅱ (AngⅡ) and cardiotrophin-1 (CT-1) in primary cultured neonatal rat cardiomyocytes. Methods: Primary cultured SD rat cardiomyocytes were cultured with modified Simpson method and whole cell extracts were prepared. The content of total protein in cardiomyocytes was determined by modified Lowry method. The myocardial cell surface area was determined by phase contrast microscopy and HJ2000 universal image analysis system. Captopril as a positive control. Results: (1) Simvastatin at a dosage of 10-6mol / L can safely and effectively inhibit the increase of total protein content of cardiomyocytes and the increase of myocardial cell surface area induced by AngⅡ, and the effect is similar to that of angiotensin converting enzyme inhibition Puli role is similar. (2) CT-1 increased the total protein content of cardiomyocytes in a dose-dependent manner. Simvastatin could significantly inhibit the increase of total cellular protein content and myocardial cell surface area induced by CT-1. Conclusion: Simvastatin can significantly inhibit the increase of myocardial total protein and the increase of myocardial cell surface area induced by Ang Ⅱ and CT-1, which has the effect of preventing and treating cardiomyocyte hypertrophy.