Liraglutide alleviates myocardial ischemia-reperfusion injury in diabetic mice

Diabetic patients are prone to acute myocardial infarction. Although reperfusion therapy can preserve the viability of the myocardium, it also causes fatal ischemia-reperfusion injury. Diabetes can exacerbate myocar-dial ischemia-reperfusion injury, but the mechanism is unclear. We aimed to characterize the effects of lir-aglutide on the prevention of ischemia-reperfusion injury and inadequate autophagy. Liraglutide reduced the myocardial infarction area and improved cardiac function in diabetic mice. We further demonstrated that lir-aglutide mediated these protective effects by activating AMPK/mTOR-mediated autophagy. Liraglutide markedly increased p-AMPK levels and the LC3 II/LC3 I ratio and reduced p-mTOR levels and p62 expression. Pharma-cological inhibition of mTOR increased cell viability and autophagy levels in high glucose and H/R-treated H9C2 cells. Overall, our study reveals that liraglutide acts upstream of the AMPK/mTOR pathway to effectively counteract high glucose-and H/R-induced cell dysfunction by activating AMPK/mTOR-dependent autophagy, providing a basis for the clinical prevention and treatment of ischemia-reperfusion in diabetes.

Automated summary

Diabetic patients are prone to acute myocardial infarction, but liraglutide can reduce myocardial injury and improve cardiac function. This study shows that liraglutide exerts its protective effects through activation of AMPK/mTOR-mediated autophagy.