紅景天苷通過促進心肌細胞肌漿網(wǎng)釋放Ca²⁺，增強心肌收縮力，又可上調(diào)肌漿網(wǎng)鈣泵的表達和下調(diào)鈣調(diào)神經(jīng)磷酸酶的表達，促進Ca²⁺返回肌漿網(wǎng)，阻滯鈣超載引起的心肌損傷，有利于改善心功能。紅景天苷通過抗氧化和抗炎作用，抑制心臟脂質(zhì)過氧化反應(yīng)，提高心臟組織的抗氧化酶活性，抑制炎性細胞因子表達和線粒體通透性轉(zhuǎn)換孔開放，阻滯心肌細胞凋亡；也可通過上調(diào)缺氧誘導(dǎo)因子和血管內(nèi)皮生長因子表達，促進缺血心肌血管形成，改善心肌缺血；還通過上調(diào)PGC-1α-NRF-1/NRF-2表達的通路，改善心肌線粒體呼吸功能，最終產(chǎn)生心臟保護作用。基于上述作用機制，紅景天苷可對抗缺氧、缺血、缺血再灌注、力竭運動、化學品、生物毒素等引起的心臟損傷。

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.