Galectin-3 knock down inhibits cardiac ischemia-reperfusion injury through interacting with bcl-2 and modulating cell apoptosis.

Acute myocardial infarction (AMI) is a fetal cardiovascular disease with high morbidity and mortality worldwide. In the present study, we elucidated the role of galectin-3 in preventing myocardial ischemic reperfusion injury. We found that galactin-3 was significantly up-regulated in the myocardium and cardiomyocyte subjected to ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) treatment, respectively. Galectin-3 knockdown significantly decreased the ischemic size of the left ventricular and the apoptosis of cardiomyocytes. Moreover, galectin-3 knockdown reversed the decrease of mitochondrial membrane potential and inhibited the inflammation response in myocardium and cultured cardiomyocyte induced by I/R and H/R, respectively. Further, this study revealed that galectin-3 interacted with bcl-2, instead of bax, in the cardiomyocyte, and regulated the phosphorylation of AKT, p70s6k, JNK, IκB and p65. Our findings demonstrated that galectin-3 could prevent myocardial I/R injury through interacting with bcl-2.

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