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目的:在原代培养的新生大鼠心肌细胞上,观察丹参酮ⅡA对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的肥大心肌细胞C-jun氨基末端激酶(C-junN-terminalkinases,JNKs)表达的影响。方法:采用相差显微镜测量心肌细胞直径大小,3H-亮氨酸掺入法测定心肌细胞蛋白质合成速率作为心肌细胞肥大的指标,用细胞免疫荧光标记和蛋白质印迹法(westernblot)检测心肌细胞核内磷酸化JNKs(JNK-P)的表达代表JNKs活性。结果:AngⅡ诱导心肌细胞肥大,其导致的心肌细胞直径、蛋白合成速率、细胞内JNK-P蛋白含量均明显高于对照组(P<0.05或P<0.01),丹参酮ⅡA对此有一定的抑制作用(P<0.05),其效果与AngⅡ受体阻滞剂氯沙坦相似。结论:丹参酮ⅡA对AngⅡ诱导的心肌细胞肥大有一定的抑制作用。其作用机制可能与丹参酮能抑制AngⅡ1型受体激活,阻止Ca2+内流,阻断丝裂原活化的蛋白激酶通路,抑制JNKs的磷酸化和向核内移位有关。
OBJECTIVE: To investigate the effect of tanshinone II A on the expression of C-jun N-terminal kinases (JNKs) in hypertrophic cardiomyocytes induced by angiotensin II (Ang II) on primary cultured neonatal rat cardiomyocytes. Methods: The diameter of myocardial cells was measured by phase contrast microscopy. The protein synthesis rate of myocardial cells was measured by 3H-leucine incorporation method as an indicator of myocardial cell hypertrophy. The nuclear phosphorylation of myocardial cells was detected by immunofluorescence labeling and western blot. Expression of JNKs (JNK-P) represents JNKs activity. RESULTS: AngII induced hypertrophy of cardiomyocytes, which resulted in a significant increase in myocardial cell diameter, protein synthesis rate, and intracellular JNK-P protein content (P<0.05 or P<0.01). Tanshinone IIA inhibited this phenomenon. The effect (P<0.05) was similar to that of the AngII receptor blocker losartan. Conclusion: Tanshinone II A can inhibit the hypertrophy of cardiomyocytes induced by Ang II. The mechanism of action may be related to the inhibition of AngII1 receptor activation, inhibition of Ca2+ influx, blocking of mitogen-activated protein kinase pathway, inhibition of phosphorylation of JNKs and translocation into the nucleus.