Objective: Myocardial infarction (MI) is a cause of high morbidity and mortality in the world.Sodium tanshinone ⅡA sulphonate (STS) has been widely used in Oriental medicine for treating cardiovascular diseases, however, the underlying mechanisms remain unclear.Alterations of circulating lipids and lipoproteins, increased fatty acid β-oxidation and oxidative stress play most important roles in the pathogenesis of MI.The accumulated evidence suggests that activating redox-sensitive extracellular signal-regulated kinase1/2 (ERK1/2) / Nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathwav is an interference against oxidative stress, and inhibiting over-activated AMP-activated protein kinase (AMPK) / acetyi CoA carboxylase (ACC) / camitine palmitoyltransferase (CPT) 1 pathway leads to the inhibition of increased fatty acid β-oxidation.Methods: The present study employed isoproterenol (ISO)-treated rats to elucidate whether STS possesses antidyslipidemia and anti-oxidant effects against experimental MI model, and to investigate its potential mechanisms of action.Results: Our study showed that STS could ameliorate cardiac dysfunction and variation of myocardial zymogram, preserve cell membrane integrity, up-regulate antioxidant systems, and maintain the levels of circulatory lipids driven by supramaximal doses ISO as well.Moreover, modulation of ERK1/2/Nrf2/HO-1 and AMPK/ACC/CPT1 pathways was involved in STS induced cardioprotection.Conclusions: STS exerts strong favorable cardioprotective action.Additionally, the present study also indicates that the properties of STS, such as anti-dyslipidemia, anti-oxidant and inhibition of fatty acid β-oxidation, may be the mechanisms underlying the observed results.