By increasing the release of Ca2+ from sarcoplasmic reticulum in cardiomyocytes,salidroside elevates myocardial contraction,and by up-regulation of sarcoplasmic reticulum Ca2+-ATPase expression,and down-regulation ofcalcineurin expression to promote Ca2+ return to sarcoplasmic reticulum,salidroside obstructs Ca2+ overload-induced myocardial injury,and improves heart function.Salidroside inhibits lipid peroxidation,and increases activities of enzymatic antioxidants in heart tissue,and inhibits expression of inflammatory cytokines,and mitochondrial permeability transition pore opening,thus blocks myocardial apoptosis,by anti-oxidation and anti-inflammation;salidroside improves myocardial ischemia by up-regulation of hypoxia-inducible factor and vascular endothelial growth factor expression to promote angiogenesis in ischemic myocardium;salidroside improves respiratory function of mitochondria in myocardium by stimulating PGC-1 αt-NRF-1/NRF-2 signaling pathway to produce finally cardioprotective effect.These effects of salidroside are thought that are major mechanism of antagonizing cardiac injury induced by hypoxia,ischemia,ischemic-reperfusion,exhaustive exercise,chemicals,and biologic toxin.