Abstract
Cardiovascular diseases, a class of the most common diseases, seriously threaten human health, which is a direct inducement of death in most countries. The restoration of blood supply is an impactful intervention way for cardiovascular disease treatments while the injury induced by oxygen-glucose deprivation and ischemic reperfusion (I/R) may further impact the tissues of the patients. Myocardial reperfusion is a precondition for saving ischemic myocardial tissues in acute myocardial infarction while the injury induced by immediate reperfusion takes a great challenge for cardiovascular disease treatment. Howbeit, the reperfusion of coronary blood could aggravate the injury triggered by ischemia. At present, several studies have focused on the etiopathogenesis and therapeutic strategies of ischemia-reperfusion injury of the myocardium. The report has verified that miR-211-5p was elevated in the pathological specimens, while the influence of miR-211-5p in I/R-mediated injury of myocardial cells remains unclear. This research is aimed at illustrating the role of miR-211-5p in the progression of I/R injury of myocardial cells, and qRT-PCR, western blot, CCK-8, and TUNEL assay were used to investigate the functions of miR-211-5p on I/R-mediated injury of myocardial cells. The result mirrored that miR-211-5p was distinctly reduced in the I/R-induced AC16, and reduced miR-211-5p could evidently improve the viability of I/R-induced AC16. miR-211-5p could directly target FBXW7, and FBXW7 upregulation could reverse the improvement of AC16 in viability and apoptosis level after suffering I/R. Moreover, it was also proved that miR-211-5p can mediate the activation of Wnt/β-catenin via attenuating FBXW7. Consequently, this investigation identified miR-211-5p as a positive role to attenuate the injury of myocardial cells when suffering I/R treatment.