Puerarin Protects Myocardium From Ischaemia/Reperfusion Injury by Inhibiting Ferroptosis Through Downregulation of VDAC1

Despite improvements in interventional techniques leading to faster myocardial reperfusion postmyocardial infarction, there has been a significant rise in the occurrence of myocardial ischaemia/reperfusion injury (MI/RI). A deeper understanding of the underlying mechanisms of MI/RI could offer a crucial approach to reducing myocardial damage and enhancing patient outcomes. This study examined the myocardial protective properties of puerarin (PUE) in the context of MI/RI using hypoxia/reoxygenation (H/R) or ischaemia/reperfusion (I/R) injury models were employed in H9c2 cells and C57BL/6 mice. Our findings demonstrate that pretreatment with PUE effectively mitigated cardiomyocyte Ferroptosis, restored redox balance, preserved mitochondrial energy production and maintained mitochondrial function following MI/RI. Furthermore, these cardioprotective effects of PUE were found to be mediated by the downregulation of voltage-dependent anion channel 1 (VDAC1) protein. These data reveal a novel mechanism by which PUE inhibits MI/RI and reveal that this protective effect of PUE is dependent on the downregulation of VDAC1.

VDAC1; ferroptosis; mitochondria; myocardial ischaemia–reperfusion injury; puerarin.