Sevoflurane preconditioning protects against acute MI/R injury via enhancing AdipoR1-Cav3 interaction and alleviating endoplasmic reticulum stress

Whether and how sevoflurane preconditioning (SevoPre) exerts protection against acute myocardial ischemia/ reperfusion (MI/R) injury remains elusive. We observed significant myocardial injury, as evidenced by infarct size, cardiomyocyte apoptosis, and circulating troponin-I, at 3 h of MI/R in both wildtype and adiponectin knockout mice. The injury was significantly ameliorated by SevoPre in wildtype mice, but not in adiponectin knockout mice. In wildtype mice, we found that MI/R could increase endoplasmic reticulum stress of car-diomyocytes, and impair association of adiponectin receptor 1 and ceveolin-3, both of which processes were largely restored by SevoPre. In summary, we demonstrated that significant injury had already took place at 3 h of MI/R, which could be ameliorated by SevoPre via promoting affinity of adiponectin receptor 1 and ceveolin-3, and then attenuating endoplasmic reticulum stress of cardiomyocytes.

Automated summary

This study found that significant injury had occurred at 3 hours of myocardial ischemia/reperfusion (MI/R), which could be alleviated by Sevoflurane preconditioning (SevoPre) through enhancing the affinity between adiponectin receptor 1 and caveolin-3, and reducing endoplasmic reticulum stress in cardiomyocytes.