4.3 Article Retracted Publication

被撤回的出版物: Influence of sodium ferulate on miR-133a and left ventricle remodeling in rats with myocardial infarction (Retracted article. See vol. 42, 2023)

Journal

HUMAN & EXPERIMENTAL TOXICOLOGY
Volume 40, Issue 3, Pages 417-424

Publisher

SAGE PUBLICATIONS LTD
DOI: 10.1177/0960327120950006

Keywords

Sodium ferulate; miR-133a; left ventricle remodeling; myocardial infarction; ischemia reperfusion

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The study found that sodium ferulate can improve cardiac hemodynamic indices, reduce infarction size and left ventricular remodeling, decrease serum malondialdehyde levels, increase antioxidant enzyme activities, and enhance miR-133a expression in myocardial tissue.
To explore the influence of sodium ferulate (SF) on miR-133a and left ventricle remodeling (LVR) in rats with myocardial infarction (MI). The left coronary artery was ligated to create 36 ischemia-reperfusion (IR) rat models that were randomly divided into mock surgical group (MSG) (not ligated), model group (MG), and sodium ferulate group (SFG). After the successful modeling, SFG was intravenously injected with SF at the dose of 10 mg/kg, and the other two groups were injected with the same volume of normal saline. After 28 days, cardiac hemodynamic indices of all groups were measured; the myocardial infarction size (MIS), left ventricular mass index (LVMI), and collagen volume fraction (CVF) were calculated, the content of serum malondialdehyde (MDA) and activities of catalase (CAT), superoxide dismutase (SOD) and glutathione catalase (GSH-px) were detected by ELISA, and miR-133a expression in myocardial tissues of the left ventricle (LV) was detected by RT-qPCR. SF improved the cardiac hemodynamic indices of rat model and reduced the MIS, LVMI and CVF. SF decreased the serum MDA level and increased the serum CAT, SOD and GSH-px levels in rat model. SF increased the expression of miR-133a in myocardial tissue of rat model. Therefore, SF could effectively reduce the myocardial injury of IR rats and improve the LVR. Its mechanism may be related to the antioxygenation and upregulation of miR-133a.

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