FULLEROL alleviates myocardial ischemia-reperfusion injury by reducing inflammation and oxidative stress in cardiomyocytes via activating the Nrf2/HO-1 signaling pathway.

OBJECTIVE

Myocardial ischemia-reperfusion injury (MIRI) is myocardial tissue injury caused by blood supply returning to myocardial tissue after ischemia or hypoxia. The purpose of this study was to investigate the protective effect of FULLEROL on myocardial tissue in MIRI rats and its mechanism.

MATERIALS AND METHODS

We use rats and ligate their left anterior descending coronary artery to make a MIRI model, and we also subcutaneously injected some MIRI rats with FULLEROL daily for two weeks before modeling. We determined the effects of model building and the therapeutic effect of FULLEROL on MIRI by detecting the changes of myocardial tissue morphology, myocardial injury markers and cardiac function in rats. In addition, we detected the expression changes of inflammatory factors and antioxidative molecules in rat myocardial tissue and serum to determine the effect of FULLEROL on inflammation and oxidative stress in myocardial tissue. Finally, we detected the activity of the Nrf2/HO-1 signaling pathway in rat cardiomyocytes to determine the mechanism of action of FULLEROL.

RESULTS

The structure of myocardial tissue in MIRI rats was remarkably damaged, and the range of myocardial infarction was increased. In addition, the concentrations of creatine kinase and lactate dehydrogenase were increased, and the heart function was reduced, while FULLEROL could reverse these conditions. In addition, FULLEROL was found to reduce the concentration of the inflammatory factors in rat myocardial tissue and serum, and to increase the expression of antioxidative molecules in myocardial tissue. The Nrf2/HO-1 signaling pathway was found to be related to MIRI and FULLEROL could increase the activity of the Nrf2/HO-1 signaling pathway in cardiomyocytes.

CONCLUSIONS

FULLEROL can alleviate MIRI by promoting the activity of the Nrf2/HO-1 signaling pathway to reduce the expression of inflammatory factors in rats and increase the antioxidative capacity of cardiomyocytes.