摘要
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.
出处
《中华急诊医学杂志》
CAS
CSCD
2007年第6期583-586,共4页
Chinese Journal of Emergency Medicine
基金
国家自然科学基金(30500657)