Moderate-intensity aerobic exercise inhibits cell pyroptosis to improve myocardial ischemia-reperfusion injury.

Abstract

Myocardial ischemia-reperfusion injury (MI/RI) significantly impacts the patients with acute myocardial infarction (AMI), with the NLRP3-mediated necrosis exacerbates the pathological progression of myocardial infarction. Exercise, recognized as a crucial approach for both disease prevention and treatment, is widely utilized in clinical practice worldwide and has demonstrated broad effectiveness in cardiovascular disease (CVD) prevention. To explore the cardio protective effect of exercise preconditioning and the mechanism by which exercise modulation of NLRP3 improves myocardial ischemia and reperfusion injury. In this study, C57BL/6N mice were employed to establish an exercise preconditioning model and a MI/RI model. The exercise intervention involved moderate-intensity aerobic exercise on a treadmill (50-70% VO2max) for small animals. Our research findings indicate that moderate-intensity aerobic exercise intervention improved cardiac function, reduced myocardial injury and inflammatory response, decreased myocardial infarction area and degree of cell apoptosis in mice compared to those raised under conventional conditions. Additionally, the expression of NLRP3 in the myocardial tissue of mice with MI/RI was reduced after exercise intervention. Moreover, exercise inhibited the activation of apoptosis related proteins such as Caspase-1 and GSDMD, while reducing the levels of inflammatory factors such as IL-1β and IL-18. This study found that moderate-intensity aerobic exercise can reduce the inflammatory response, reduce the degree of cell pyroptosis, reduce myocardial ischemia and reperfusion injury, and achieve endogenous protective effects on the myocardium.