miR-124 regulates myocardial ischemia reperfusion injury

Objective: To study the role of miR-124 in myocardial ischemia-reperfusion induced cardiomyocyte injury by targeted regulation of beclin 1 (BECN 1). Method: The rat model of myocardial ischemia-reperfusion was established. The rats were divided into the miR-124 group (injected with miR-124 inhibitor), the MIRI group (not treated), and the miR-NC group (injected with miR-NC). Meanwhile, blank group and sham operation groups were set up. LDH and CK in the five groups were detected by ELISA at 12 h after operation. The myocardial infarct size of each group was measured by multimedia color pathological analysis. Then, an in vitro cell model was established. First, the rat cardiomyocytes were isolated, extracted and cultured; then miR-124 was transfected into the cells, the test group cells were transfected with miR-124, and the miR-NC were transfected into cells. NC cells were set as negative control group, and cells not transfected were set as blank control group. Then, an in vitro cell model was established. First, the rat cardiomyocytes were isolated, extracted and cultured, then cells transfected with miR-124 and miR-NC were set as test group and negative control group, and cells not transfected were set as blank control group. The relative expression of miR-124 in rat myocardium as well as in cardiomyocytes transfected with miR-124 were measured. Western blot was applied to analyze the relative expression levels of Beclin-1 and LC3B proteins in cardiomyocytes and flow cytometry was used to analyze the apoptosis of cells. Results: There were no significant differences in serum CK and LDH levels between the blank group, the sham operation group and the miR-124 group after modeling (P>0.05), but those of the MIRI group and the miR-NC group were significantly higher than that in the blank group, the sham operation group and the miR-124 group (P<0.05). The miR-124 in the myocardial tissue of the blank group, the sham operation group and the miR-124 group were significantly lower than those of the MIRI group and the miR-NC group (P<0.05). There was no significant difference in Beclin 1 mRNA expression among the five groups (P>0.05). The myocardial infarct size of the miR-124 group was significantly smaller than that of the MIRI group and the miR-NC groups (P<0.05). For in vitro results, the expression of miR-124 after transfection in the myocardial cells of the test group was significantly higher than that in the blank group and the negative control group (P<0.05). The expression levels of Bclin 1 and LC3 autophagy in the cardiomyocytes of the test group were significantly lower than those of the blank and negative control groups (P<0.05). The apoptosis rate of cardiomyocytes in the test group was also significantly higher than that in the blank group and the negative control group (P<0.05). Conclusion: miR-124 is highly expressed in MIRI and may reduce the level of autophagy and promote apoptosis through competitive binding of BECN 1, which may be an important target for MIRI treatment in the future.