MiR-26a inhibits myocardial cell apoptosis in rats with acute myocardial infarction through GSK-3β pathway

S. Lu, Y. Lu

Department of Emergency Medicine, First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China. 346568533@qq.com

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• Cardiology

OBJECTIVE: To study the influence of micro ribonucleic acid (miR)-26a on myocardial cell apoptosis in rats with acute myocardial infarction (AMI) through the glycogen synthase kinase 3 beta (GSK-3β) pathway.

MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12), and miR-26a mimics group (n=12). Only the heart was exposed, and normal saline was intraperitoneally injected postoperatively in sham group, and the model of AMI was prepared in model group. Besides, after modeling, miR-26a mimics were injected into the left ventricle in miR-26a mimics group. At 48 h after operation, sampling was performed. Then, the expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax), as well as the protein expression of phosphorylated GSK-3β (p-GSK-3β) were detected via immunohistochemistry and Western blotting, respectively. Moreover, the expression level of miR-26a was measured via quantitative polymerase chain reaction (qPCR), and cell apoptosis was evaluated using terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay.

RESULTS: Compared with those in sham group, the expression level of Bax was substantially raised, but that of Bcl-2 was notably lowered in model group and miR-26 mimics group (p<0.05), and miR-26 mimics group had a markedly lower expression level of Bax and a remarkably higher expression level of Bcl-2 than model group (p<0.05). According to Western blotting results, the protein expression level of p-GSK-3β in model and miR-26a mimics groups was considerably higher than that in sham group (p<0.05), and miR-26a mimics group exhibited a notably higher protein expression level of p-GSK-3β than model group (p<0.05). In comparison with that in sham group, the expression level of miR-26a rose markedly in both model group and miR-26a mimics group (p<0.05), and its expression level in miR-26a mimics group was dramatically higher than that in model group (p<0.05). Additionally, the TUNEL-positive cells were considerably increased in both model group and miR-26a mimics group in comparison with that in sham group (p<0.05), and miR-26a mimics group had markedly fewer TUNEL-positive cells than model group (p<0.05).

CONCLUSIONS: MiR-26a activates the GSK-3β signaling pathway to inhibit myocardial cell apoptosis after AMI.

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