Key result
Sodium tanshinone IIA sulfonate reduces infarct size and apoptosis after MI by inhibiting JNK activation.
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.
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Yang et al. (2008) studied Acute myocardial infarction and cardiomyocyte apoptosis. Sodium tanshinone IIA sulfonate (STS) vs. No STS treatment (MI or H2O2 only) was evaluated on Infarct size, blood lactate dehydrogenase (LDH) level, and cardiomyocyte apoptosis. Sodium tanshinone IIA sulfonate significantly reduced infarct size, blood LDH levels, and cardiomyocyte apoptosis in rat models of myocardial infarction by inhibiting JNK activation.
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