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目的:在原代培养的新生大鼠心肌细胞上,探讨血管紧张素Ⅱ(AngⅡ)诱导的心肌细胞c-fos,c-junmRNA表达变化及丹参酮ⅡA的影响。方法:取12只1 d龄新生Wistar乳鼠,进行心肌细胞培养,分为正常对照组,AngⅡ(10-6mol.L-1)组,AngⅡ(10-6mol.L-1)+丹参酮ⅡA(10-8g.L-1)组,AngⅡ(10-6mol.L-1)+缬沙坦(10-6mol.L-1)组,丹参酮ⅡA(10-8g.L-1)组,缬沙坦(10-6mol.L-1)组。相差显微镜测量心肌细胞大小,[3H]-亮氨酸掺入法测定心肌细胞蛋白质合成速率;RT-PCR检测心肌细胞c-fos,c-jun mRNA的表达。结果:在培养液中加入AngⅡ作用30 min后,心肌细胞c-fos,c-jun mRNA的表达显著增强(P<0.01);AngⅡ作用24 h后,AngⅡ组心肌细胞蛋白质合成速率较对照组明显增加(P<0.01);AngⅡ持续作用7 d后,AngⅡ组心肌细胞直径较对照组显著增大(P<0.05)。采用丹参酮ⅡA或缬沙坦干预,二者可抑制AngⅡ诱导的c-fos,c-jun mRNA的表达增强(P<0.01)、心肌细胞蛋白质合成速率的增加(P<0.01)及心肌细胞直径增大(P<0.05)。结论:丹参酮ⅡA可通过抑制AngⅡ诱导的心肌细胞c-fos,c-jun的表达增强,减轻心肌肥大。
OBJECTIVE: To investigate the changes of c-fos and c-jun mRNA expressions in cardiomyocytes induced by angiotensin Ⅱ (AngⅡ) and the effect of tanshinone Ⅱ A on primary cultured neonatal rat cardiomyocytes. Methods: Twelve newborn Wistar neonatal rats (1 d) were used in this study. Cardiomyocytes were cultured and divided into normal control group, AngⅡ (10-6mol.L-1) group, AngⅡ (10-6mol.L-1) (10-6mol.L-1) + valsartan (10-6mol.L-1) group, tanshinoneⅡA (10-8g.L-1) group, valsartan Tan (10-6mol.L-1) group. The myocardial cell size was measured by phase-contrast microscopy. The protein synthesis rate of cardiomyocytes was measured by [3H] -leucine incorporation method. The expression of c-fos and c-jun mRNA was detected by RT-PCR. Results: The expressions of c-fos and c-jun mRNA in cardiomyocytes were significantly increased after AngⅡ treatment for 30 min (P <0.01). After AngⅡ treatment for 24 h, the protein synthesis rate in AngⅡ group was significantly higher than that in control group (P <0.01). After Ang Ⅱ continued for 7 days, the diameter of myocardial cells in AngⅡgroup was significantly increased (P <0.05). Tanshinone ⅡA or valsartan intervention could inhibit the expression of c-fos and c-jun mRNA induced by AngⅡ (P <0.01), increase the protein synthesis rate of cardiomyocytes (P <0.01) and increase of myocardial cell diameter Large (P <0.05). Conclusion: Tanshinone ⅡA can inhibit cardiac hypertrophy by inhibiting the expression of c-fos and c-jun induced by Ang Ⅱ.