Tongmai Yangxin pills alleviate myocardial ischemia-reperfusion injury by enhancing mitochondrial function via activating the ERK signaling pathway.

BACKGROUND

To explore the mechanism of Tongmai yangxin pills (TMYX) for improving myocardial ischemia-reperfusion injury (MIRI) in rats.

METHODS

In a SD rat model of MIRI, the therapeutic effects of TMYX were evaluated by cardiac echography, measurement of myocardial infarction area, and examination of myocardial pathology, myocardial enzymes, and serum levels of inflammatory cytokines. In cultured H9c2 cells, the protective effects of aqueous extract of TMYX in the presence or absence of an ERK inhibitor against hypoxia/reoxygenation (H/R) injury and on mitochondrial function were evaluated by assessing cell viability, apoptosis, reactive oxygen species (ROS) levels, cytoplasmic and mitochondrial Ca²⁺ concentrations, mitochondrial membrane potential, mitochondrial permeability transition pore (mPTP) opening, and mitochondrial respiration. The mitochondria-related indicators were measured to validate the role of the ERK signaling pathway in mediating the alleviating effect of TMYX on mitochondrial function in H9c2 cells with H/R injury.

RESULTS

In rat models of MIRI, TMYX significantly improved cardiac function, alleviated myocardial injury, and reduced inflammatory factor levels, oxidative stress, and myocardial infarction area. In H9c2 cells with H/R injury, TMYX treatment obviously enhanced H9c2 cell viability, increased cellular ATP and ATPase levels and mitochondrial membrane potential, and reduced cell apoptosis rate, ROS level, and mPTP opening. The application of the ERK inhibitor significantly attenuated the protective effect of TMYX on mitochondrial function of H9c2 cells with H/R injury.

CONCLUSION

TMYX alleviate MIRI in rats by promoting mitochondrial function via activating the ERK signaling pathway.