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OBJECTIVE To investigate the protective effect of salvianolic acid A(Sal A)on isoproterenol-induced myocardial infarction in mice and its possible mechanisms.METHODS The mice were subcutaneously injected with isopropranol(ISO 8mg·kg-1)to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate,electrocardiogram(ECG),heart function,myocardial infarction index,serum myocardial enzymes and explored its possible mechanisms from inflammatory,antioxidant and cells apoptosis.RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice,reduced the heart index,inhibited the myocardial enzyme leakage,showed obvious myocardial protection effects.ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6,TNF-α.Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2,reduce the expression of apoptosis protein Bax,and raise the phosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K/Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.
OBJECTIVE To investigate the protective effect of salvianolic acid A (Sal A) on isoproterenol-induced myocardial infarction in mice and its possible mechanisms. METHODS The mice were subcutaneously injected with isopropranol (ISO 8 mg · kg-1) to induce myocardial infarction and evaluated the myocardial protective effect of Sal A from mortality rate, electrocardiogram (ECG), heart function, myocardial infarction index, serum myocardial enzymes and explored its possible mechanisms from inflammatory, antioxidant and cells apoptosis. RESULTS Sal A can dose-dependently enhanced the heart function of myocardial infarction mice, reduced the heart index, inhibited the myocardial enzyme leakage, showed obvious myocardial protection effects. ELISA results showed that Sal A can reduce the expression of myocardial inflammatory cytokines such as IL-6, TNF-α. Western blotting confirmed that Sal A can increase the expression of anti-apoptotic proteins Bcl-2, reduce the expression of apoptosis protein Bax, and raise the p hosphorylation level of PI3K and Akt.CONCLUSION Sal A have displayed significant protective effect against isoproterenol-induced myocardial infarction and its mechanism may be related to increasing of PI3K / Akt signal pathway and inhibition of cell apoptosis and inflammatory reaction.