Puerarin Alleviates Myocardial Ischemia-Reperfusion Injury by Enhancing FUNDC1-Mediated Mitophagy
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Background Myocardial ischemia‑reperfusion injury (MI/RI) is a major contributor to adverse outcomes in ischemic heart disease. Mitochondrial dysfunction plays a central role in MI/RI, and modulating mitophagy has shown potential in attenuating such injury. Nevertheless, whether puerarin influences mitophagy during MI/RI remains poorly understood. Methods An in vivo MI/RI model (I 30min /R 24h ) was established in C57BL/6 mice after 7‑day puerarin pretreatment. In vitro, a hypoxia‑reoxygenation (H/R) model (H 8h /R 4h ) was constructed using H9c2 cardiomyocytes. Cardiac function was assessed by echocardiography, infarct size was determined via Evans Blue‑TTC staining, mitophagy was visualized by transmission electron microscopy (TEM), and expression of mitophagy‑related proteins was evaluated by western blot. Results Puerarin significantly reduced I/R‑induced damage in both models. It attenuated mitochondrial depolarization and reactive oxygen species (ROS) generation, increased mitophagic activity, and upregulated the mitophagy receptor FUNDC1. Conclusion Puerarin alleviates myocardial ischemia‑reperfusion injury by enhancing FUNDC1‑mediated mitophagy, particularly during early reperfusion. These
