Effect and mechanism of gomisin D on the isoproterenol induced myocardial injury in H9C2 cells and mice

Abstract

We established myocardial injury models in vivo and in vitro to investigate the cardioprotective effect of gomisin D obtained from Schisandra chinensis. Gomisin D significantly inhibited isoproterenol-induced apoptosis and hypertrophy in H9C2 cells. Gomisin D decreased serum BNP, ANP, CK-MB, cTn-T levels and histopathological alterations, and inhibited myocardial hypertrophy in mice. In mechanisms research, gomisin D reversed ISO-induced accumulation of intracellular ROS and Ca²⁺. Gomisin D further improved mitochondrial energy metabolism disorders by regulating the TCA cycle. These results demonstrated that gomisin D had a significant effect on isoproterenol-induced myocardial injury by inhibiting oxidative stress, calcium overload and improving mitochondrial energy metabolism.

Keywords:

• Gomisin D
• isoproterenol
• myocardial injury
• myocardial hypertrophy
• mitochondrial energy metabolism

Acknowledgments

All work was finished in the Institute of Materia Medica, Chinese Academy of Medical Science.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This project was financially supported by the National Key Research and Development Program of China (No. 2019YFC1708901) and CAMS Innovation Fund for Medical Sciences (CIFMS, Nos. 2021-I2M-1-028 and 2021-I2M-1-029).