Abstract:
OBJECTIVE:Myocardial infarction (MI), which causes irreversible damage and loss of cardiomyocytes, is the most important cause of death in the world. MicroRNA is an important regulator of physiological and pathological activities of cardiovascular system. The aim of this research was to study the effect of microRNA-323-3p (miR-323-3p) on MI and its underlying mechanisms of action. MATERIALS AND METHODS:A rat model of MI was established to measure the expression of miR-323-3p, Bax, Bcl-2, SOD1, and SOD2 in ischemic myocardial tissue, and the cardiac function of rats were tested at seventh day after MI. H9c2 cells were divided into control group, miRNA negative control (NC) transfection group, miR-323-3p mimic (miR-323-3p min) transfection group, and then, treated with H2O2. Oxidative stress and apoptosis of H9c2 cells were observed by Western blot, Real Time-Polymerase Chain Reaction (RT-PCR), flow cytometry, SOD activity assay, TUNEL staining, DHR dye assay, etc. RESULTS: The level of miR-323-3p was decreased in ischemic myocardium, as well as H2O2-treated H9c2 cells. MiR-323-3p overexpression greatly decreased the level of Bax and increased the levels of SOD1, SOD2, and Bcl-2. After treated with miR-323-3p mimic, TUNEL positive cells were greatly reduced, and apoptosis rate of H9c2 cells was greatly decreased. Moreover, SOD levels significantly increased, while ROS production decreased after treatment of miR-323-3p. After intravenous injection of miR-323-3p agomir in rats with MI, the cardiac function of the rats was significantly improved. Western blot and Luciferase reporter gene experiments illustrated that miR-323-3p acts by targeting TGF-β2. CONCLUSIONS:MiR-323-3p was downregulated in ischemic myocardium and H2O2-treated H9c2 cells, and miR-323-3p overexpression reduced oxidative stress and apoptosis of cardiomyocytes. The protective function was achieved via regulation of TGF-β2/JNK pathway.
journal_name
Eur Rev Med Pharmacol Scijournal_title
European review for medical and pharmacological sciencesauthors
Shi CC,Pan LY,Zhao YQ,Li Q,Li JGdoi
10.26355/eurrev_202006_21688subject
Has Abstractpub_date
2020-06-01 00:00:00pages
6961-6970issue
12eissn
1128-3602issn
2284-0729journal_volume
24pub_type
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journal_title:European review for medical and pharmacological sciences
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更新日期:2012-04-01 00:00:00
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journal_title:European review for medical and pharmacological sciences
pub_type: 杂志文章,meta分析
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更新日期:2017-01-01 00:00:00