丹参酮ⅡA对血管紧张素Ⅱ诱导的心肌肥大c-fos和c-jun mRNA表达的影响

Effects of tanshinoneⅡ on the expression of c-fos and c-jun in angiotensin Ⅱ-induced hypertrophy of cardiomyocytes

目的在原代培养的新生大鼠心肌细胞上，观察丹参酮ⅡA（tanshinoneⅡ，TSN）对血管紧张素Ⅱ（angiotensinⅡA，AngⅡ）诱导的心肌细胞肥大的影响。方法采用相差显微镜测量细胞大小，测定心肌细胞’H．亮氨酸掺入作为心肌细胞肥大的指标；用逆转录聚合酶链式反应（RTPCR）检测心肌细胞原癌基因c-fos和c—jun mRNA的表达，MTT法检测细胞活力。结果培养的心肌细胞中加入TSN（5～80μmol／L），24h后没有产生明显的细胞毒性。TSN能抑制AngⅡ诱导的心肌细胞增大、蛋白质合成速率的显著增加及心肌细胞原癌基因c—fos和c-jun mRNA表达的增强。结论TSN可以抑制AngⅡ诱导的心肌细胞肥大，这可能与其抑制了原癌基因c-fos和c-jun的表达有关。

Objective To investigate the effect of Tanshinone Ⅱ A （TSN） on the cell hypertrophy induced by angiotensin H （ Ang Ⅱ ） in the primary culture of neonatal rat cardiomyocytes. Method The effect of TSN on cardiomyocyte was evaluated by the 3- [4, 5-dimethyhhiazol-2-yl] -3, 5-diphenylformazan （MTT） assay. As the index of cardiomyocyte hypertrophy, protein synthesis rate was measured by ^1H-Leucine incorporation and the cell size was determined by phase contrast microscope. The proto-oncogene c-fos mRNA and c-jun mRNA expression was assessed using reverse transcription polymerase chain reaction （RT-PCR）. Results Exposure of the myocytes to TSN （5 - 80 mmol/L） for 24hours produced no cytotoxicity. Protein synthesis rate and proto-oncogene c-los and c-Jun mRNA expression of cardinmyocytes increased significantly after Ang Ⅱ treatment, and TSN inhibited these effect of Ang 11 . Conclusions TSN can prevent the hypertrophy of cardiomyocytes induced by Ang Ⅱ , which be attributable relate to the decreased expression of proto-oneogene c-fos and c-jun mRNA by TSN.