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丹参酮ⅡA抑制心肌肥厚的机制研究 被引量:8

The mechanism of positive effect of tanshinone ⅡA on cardiac hypertrophy
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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(tanshinoneⅡA,TSN)对血管紧张素Ⅱ(angiotensinⅡA,AngⅡ)诱导的心肌细胞肥大的影响及可能机制。方法采用流式细胞仪测定心肌细胞总蛋白含量作为心肌细胞肥大的指标;用逆转录聚合酶链式反应(RT-PCR)检测心肌细胞原癌基因c-fosmRNA的表达,并用显微荧光分光光度仪测定[Ca2+]I。结果TSN能抑制AngⅡ诱导的心肌细胞蛋白质含量的显著增加(P<0·05)、心肌细胞原癌基因c-fosmRNA表达的增强(P<0·05)及[Ca2+]I的增加,其效果与AngⅡ受体阻滞剂缬沙坦(valsartan,Val)相似。结论TSN可以抑制AngⅡ诱导的心肌细胞肥大及原癌基因c-fos的表达,这与其抑制AngⅡ诱导的心肌细胞[Ca2+]I的增加有关。 Objective To investigate the effect and the mechanism of tanshinone Ⅱ A(TSN) on the hypertrophy induced by angiotensin Ⅱ (Ang Ⅱ ) in the primary culture of neonatal rat cardiomyocytes. Methods As the index of cardiomyocyte hypertrophy, cellular protein content of cardiomyocyte was analysed with flow cytometric analysis. The proto-oncogene c-fos mRNA expression was assessed using reverse transcription polymerase chain reaction(RT-PCR) and [Ca^2+]Ⅰ was measured by fluorescent spectromicroscope system. Results Cellular protein content and proto-oncogene c-fos mRNA expression of cardiomyocytes and [Ca^2+]Ⅰ increased significantly after Ang Ⅱ treatment,and TSN inhibited these effects of Ang Ⅱ . Conclusion TSN can prevent the hypertrophy of cardiomyocytes induced by Ang Ⅱ ,which may relate to the decreased expression of proto-oncogene c-fos mRNA which resulted from decreased [Ca^2+]Ⅰ by TSN.
出处 《中国基层医药》 CAS 2005年第7期775-776,共2页 Chinese Journal of Primary Medicine and Pharmacy
关键词 血管紧张素II 丹参酮ⅡA 心肌细胞肥大 c—fos基因 Tanshinone Ⅱ A Angiotensin Ⅱ Cardiomyocyte hypertrophy Genes c-fos
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  • 1Sadoshima J, Izumo S. Molecular characterization of angiotensin Ⅱ -induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype. Cre Res, 1993,73:413-423.
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