Sodium tanshinone IIA sulfonate protects cardiomyocytes against oxidative stress-mediated apoptosis through inhibiting JNK activation

被引：182

作者：

Yang, Ruifang ^{[1
]}

Liu, Aijun ^{[1
]}

Ma, Xiujuan ^{[1
]}

Li, Lin ^{[1
]}

Su, Dingfeng ^{[1
]}

Liu, Jianguo ^{[1
]}

机构：

[1] Second Mil Med Univ, Sch Pharm, Dept Pharmacol, Shanghai 200433, Peoples R China

来源：

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY | 2008年 / 51卷 / 04期

关键词：

sodium tanshinone IIA sulfonate; myocardial infarction; oxidative stress; apoptosis; JNK;

D O I：

10.1097/FJC.0b013e3181671439

中图分类号：

R5 [内科学];

学科分类号：

1002 [临床医学]; 100201 [内科学];

摘要：

Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA, a well-known Chinese medicine for treating cardiovascular disorders. Cardiomyocyte apoptosis plays a major role in the development of cardiovascular diseases. The present study was designed to investigate the effects of STS on cardiomyocyte apoptosis induced by in vivo acute myocardial infarction (MI) in adult rats and by in vitro H2O2-treated neonatal rat ventricular myocytes. In MI rats, STS significantly reduced the infarct sizes, the blood lactate dehydrogenase (LDH) level, and the number of apoptotic cardiomyocytes in the infarcted hearts. In the in vitro study, STS reversed the decreased effect of cell viability induced by H2O2. In addition, STS also markedly inhibited H2O2-induced cardiomyocyte apoptosis. C-Jun N-terminal kinases/stress-activated protein kinases (JNKs/SAPKs) and p38 MAPK are classic oxidative stress activated protein kinases. Our further mechanistic study revealed that increased JNK phosphorylation stimulated by H2O2 was abolished by STS treatment. In conclusion, inhibition of JNK activation plays a significant role in cardioprotective effects of STS.

引用

页码：396 / 401

页数：6

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