The reperfusion of coronary artery blood supply is often accompanied by myocardial hypoxia/reperfusion (H/R) injury, and induced cardiomyocytes apoptosis. The activation of p38 can induce apoptosis, thereby aggravating the myocardial H/R injury. Metallothionein-2A (MT2A) has the functions of anti-apoptosis and protective effect through p38. However, it is not clear that MT2A may protect cardiomyocytes from H/R injury through p38 signaling pathway. Here, we constructed an H/R model for H9c2 cardiomyocytes to explore the protective effect of MT2A on cardiomyocytes apoptosis during the process of H/R through p38 signal pathway. The results revealed that both endogenously overexpressed MT2A and exogenously added MT2A can inhibit the active expression of p-p38 and cleaved caspase-3 under H/R. Based on our results, H/R induced cardiomyocytes apoptosis and activation of p38. And, MT2A can inhibit the active expression of caspase-3 and p38. We found that MT2A can protect cardiomyocytes apoptosis from H/R injury through p38 signaling pathway.
Keywords: Cardiomyocyte; Hypoxia/reperfusion; Metallothionein-2A; p38.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.