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.

急性心肌梗塞（AMI）是一种胎儿心血管疾病，在全世界范围内都有很高的发病率和死亡率。在本研究中，我们阐明了galectin-3在预防心肌缺血再灌注损伤中的作用。我们发现在接受缺血/再灌注（I / R）和缺氧/复氧（H / R）处理的心肌和心肌细胞中，galactin-3明显上调。Galectin-3基因敲低显着降低了左心室的缺血面积和心肌细胞的凋亡。此外，galectin-3敲低逆转了线粒体膜电位的下降，并分别抑制了I / R和H / R诱导的心肌和培养的心肌细胞的炎症反应。此外，这项研究还表明，galectin-3在心肌细胞中与bcl-2而非bax相互作用，并调节AKT，p70s6k，JNK，IκB和p65的磷酸化。我们的研究结果表明，galectin-3可通过与bcl-2相互作用来预防心肌I / R损伤。