MiR-328 inhibits cell apoptosis and improves cardiac function in rats with myocardial ischemia-reperfusion injury through MEK-ERK signaling pathway

H.-K. Ye, H.-H. Zhang, Z.-M. Tan

Department of Critical Care Medicine, Jining No. 1 People’s Hospital; Affiliated Jining No. 1 People’s Hospital of Jining Medical University, Jining Medical University, Jining, China. sandy1412@sina.com

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• Cardiology

OBJECTIVE: To explore the influences of micro ribonucleic acid (miR)-328 on rats with myocardial ischemia-reperfusion (IR) injury through the methyl ethyl ketone (MEK)/extracellular signal-regulated kinase (ERK) signaling pathway.

MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly assigned into the sham group (n=12), model group (n=12), and miR-328 group (n=12). The model of myocardial IR injury was established by ligating the left anterior descending coronary artery, without any intervention in the model group, while 200 μL of miR-328 antagomir was intravenously injected before modeling in the miR-328 group. The activity of the serum myocardial enzymes lactate dehydrogenase (LDH) and creatine kinase-muscle/brain (CK-MB) was determined via ELISA to assess the cardiac function in the three groups of rats, and the mRNA expression level of miR-328 in myocardial tissues was measured through real-time fluorescence qRT-PCR in the sham group, model group, and miR-328 group. TUNEL staining was performed to detect apoptotic cells, and the levels of myocardial apoptosis-associated protein Caspase-3 and phosphorylated MEK1/2 (p-MEK1/2) and p-ERK1/2 proteins were determined using Western blotting.

RESULTS: Compared with the sham group, the model group exhibited increased activity of LDH and CK-MB, miR-328 expression level, apoptotic cells, the relative expression level of Caspase-3, and protein levels of p-MEK and p-ERK, with statistically significant differences (p<0.05). Besides, in comparison with the model group, miR-328 group showed a decreased activity of LDH and CK-MB, miR-328 expression level, the relative expression level of Caspase-3, and protein levels of p-MEK and p-ERK, displaying statistically significant differences (p<0.05).

CONCLUSIONS: MiR-328 modulates the MEK-ERK signaling pathway to inhibit cell apoptosis and improve the cardiac function in rats with myocardial IR injury.

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