红景天苷通过促进心肌细胞肌浆网释放Ca²⁺，增强心肌收缩力，又可上调肌浆网钙泵的表达和下调钙调神经磷酸酶的表达，促进Ca²⁺返回肌浆网，阻滞钙超载引起的心肌损伤，有利于改善心功能。红景天苷通过抗氧化和抗炎作用，抑制心脏脂质过氧化反应，提高心脏组织的抗氧化酶活性，抑制炎性细胞因子表达和线粒体通透性转换孔开放，阻滞心肌细胞凋亡；也可通过上调缺氧诱导因子和血管内皮生长因子表达，促进缺血心肌血管形成，改善心肌缺血；还通过上调PGC-1α-NRF-1/NRF-2表达的通路，改善心肌线粒体呼吸功能，最终产生心脏保护作用。基于上述作用机制，红景天苷可对抗缺氧、缺血、缺血再灌注、力竭运动、化学品、生物毒素等引起的心脏损伤。

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 of calcineurin 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-1α-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.