Energy Metabolism Mechanism of Anticardiogenic Shock Effect Component Ginsenoside Rc of Shenfu Injection on H9c2 Myocardial Injury Cells Induced by HypoxiaReoxygenation

Abstract EN

Shenfu Injection (SFI) is a common drug used to treat cardiovascular diseases and has a significant effect on cardiogenic shock.

Ginsenoside Rc (G-Rc) was an anticardiogenic shock effect component of SFI screened by UHPLC-Q-TOF/MS and multivariate statistical analysis and further selected by molecular docking experiment in our previous study.

However, most studies on SFI in the treatment of cardiogenic shock focus on the overall efficacy, and little is known about its effective component on energy metabolism in hypoxia/reoxygenation- (H/R-) induced myocardial injury cells.

Therefore, the present study was performed to investigate the dose-effect and time-effect relationship of G-Rc in protecting hypoxic injury of H9c2 cardiomyocytes, and its mechanism on the energy metabolism-related indicators, i.e., adenosine triphosphate (ATP) content, lactate dehydrogenase (LDH) release, and creatine kinase (CK) activity of the myocardial cells, was explored.

In this paper, a stable and reliable H/R model of H9c2 cardiomyocytes was established.

Compared with the control group, the activity of cardiomyocytes in the H/R group was significantly reduced (P<0.01).

The dose-effect and time-effect studies showed that G-Rc could significantly increase cell viability at certain point compared with the H/R group (P<0.01), and the optimum intervention dose and time was 3.33 μmol/L for 12 h.

The results concerning energy metabolism mechanism demonstrated that G-Rc pretreatment could improve ATP content, attenuate the LDH leakage, and decrease CK activity and apoptosis rate of H/R cardiomyocytes.

Taken together, our findings suggest that G-Rc pretreatment can significantly protect myocardial cells from H/R injury.

In addition, G-Rc is able to improve the energy metabolism ability of the injury cardiomyocytes by direct synthesis of ATP and reducing the activity of LDH, CK, and apoptosis rate.

These results indicate that G-Rc may be a promising therapeutic candidate for the treatment of cardiovascular disease caused by myocardial H/R injury.