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BioMed Research International
Volume 2018, Article ID 3452748, 8 pages
https://doi.org/10.1155/2018/3452748
Research Article

The Role of miRNA-132 against Apoptosis and Oxidative Stress in Heart Failure

1General Hospital of Shenyang Military Area Command, No. 83 Wenhua Road, Shenyang, Liaoning Province 110016, China
2China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, Liaoning Province 110122, China

Correspondence should be addressed to Hongxu Jin; moc.361@321nijuxgnoh and Mingxiao Hou; moc.361@888oaixgnimuoh

Received 28 November 2017; Revised 17 January 2018; Accepted 24 January 2018; Published 25 February 2018

Academic Editor: Alfredo Conti

Copyright © 2018 Xuelei Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. To explore the effect of microRNA-132 of heart failure and provide theoretical guidance for clinical treatment of heart failure (HF). Methods. Peripheral blood was collected from HF patients. RT-qPCR was used to determine microRNA-132 expression. Mouse models of heart failure were established. Color Doppler ultrasound was utilized to measure the changes of cardiac function. HE and Masson staining were applied to observe pathological changes of the myocardium. After H9C2 cells were transfected with microRNA-132, MTT assay was employed to detect the stability of H9C2 cells. ELISA was used to measure the levels of oxidative stress factors. Western blot assay and RT-qPCR were utilized to determine the expression of Bax, Bcl-2, TGF-β1, and smad3. Results. MicroRNA-132 expression was downregulated in HF patients’ blood. After establishing mouse models of HF, cardiac function obviously decreased. HE staining revealed the obvious edema and hypertrophy of cardiomyocytes. Masson staining demonstrated that cardiomyocytes were markedly fibrotic. After microRNA-132 transfection and H9C2 cell apoptosis induced by H2O2, antioxidant stress and antiapoptotic ability of the H9C2 cells obviously increased. TGF-β1 and smad3 expression remarkably diminished. Conclusion. Overexpression of microRNA-132 dramatically increased the antioxidant stress and antiapoptotic ability of H9C2 cells and decreased the expression of TGF-β1 and smad3.