MicroRNA‑24 protects against myocardial ischemia‑reperfusion injury via the NF‑κB/TNF‑α pathway
- Chenlei Li
- Ming Fang
- Zhikang Lin
- Wenhui Wang
- Xinming Li
Affiliations: Graduate School, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China, Department of Cardiology, Shanghai University of Medicine and Health Sciences Affiliated Zhoupu Hospital, Shanghai 201318, P.R. China
- Published online on: September 13, 2021 https://doi.org/10.3892/etm.2021.10723
Copyright: © Li
et al. This is an open access article distributed under the
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Acute myocardial infarction (AMI) is a form of cardiomyopathy in which a blocked coronary artery leads to an irreversible loss of cardiomyocytes due to inadequate blood and oxygen supply to the distal myocardium tissues, eventually leading to heart failure. Recently, studies have revealed that microRNA (miRNA/miR)‑24 has diagnostic value in the pathogenesis of AMI by affecting multiple cell processes such as cell proliferation, differentiation and apoptosis. However, the specific mechanism of miR‑24 in ischemia‑reperfusion injury (IRI) after AMI remains to be fully elucidated. The present study aimed to investigate the effects and mechanisms of miR‑24 in IRI. In vitro, the current study detected cellular apoptosis and apoptotic‑related protein expression levels in the cardiomyocyte H9C2 cell line (negative control group, model group and miRNA group) via flow cytometry and western blot analysis. In the in vivo study, rats were randomly divided into sham, model and miRNA groups. The infarct area was observed using nitro blue tetrazolium staining, pathological changes of the myocardium were detected via hematoxylin and eosin staining and TUNEL staining was used to detect cardiomyocyte apoptosis. The expression levels of related proteins were evaluated via immunohistochemistry and western blot analysis. The in vitro and in vivo results demonstrated that miR‑24 significantly inhibited cardiomyocyte apoptosis compared with the model group. Concurrently, the expression levels of proteins associated with the NF‑κB/TNF‑α pathway (NF‑κB, caspase‑3, Bax, Bcl‑2, TNF‑α, vascular cell adhesion molecule 1, intercellular adhesion molecule 1 and monocyte chemoattractant protein‑1) in the miRNA group were significantly different from the model group (P<0.001). Compared with the model group, miR‑24 significantly improved pathological damage and infarct size of rat myocardium. Overall, the present results suggested that miR‑24 improves myocardial injury in rats by inhibiting the NF‑κB/TNF‑α pathway.