Liraglutide ameliorates hypoxia/reoxygenation-induced H9C2 cardiomyocyte apop-tosis via mitochondrial-cytochrome C pathway
Objective To further study the role of liraglutide in cardiomyocytes treated with hypoxia/reoxygenation(H/R)and its underly-ing mechanism.Methods A H/R model of rat myocardial cell line(H9C2)was established to simulate myocardial ischemia/reperfusion(1/R)injury in vitro.3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide(MTT)and Annexin V FITC-PI staining methods were used to measure the cell proliferation and apoptosis.Cellular oxidative stress products and mitochondrial function were detected.West-em blotting was used to detect the expression of apoptosis-related protein and the release of cytochrome C.Results Liraglutide protected H9C2 cells from H/R-induced damage,because the administration of liraglutide attenuated the effects of H/R on H9C2 cell viability,apop-tosis and reactive oxygen species(ROS)production(P＜0.05).More importantly,liraglutide protected mitochondrial function and prevented the release of cytochrome C in H9C2 cells after H/R injury(P＜0.05).Conclusion These results revealed the potential cardio-vascular protective effects of liraglutide in the treatment of I/R-related myocardial injury.
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