河北医学2025，Vol.31Issue(5)：711-717,7.DOI:10.3969/j.issn.1006-6233.2025.05.02
miR-425-5p调控ERK/Nrf2信号通路介导的氧化损伤抑制大鼠心力衰竭
miR-425-5p-Mediated Regulation of ERK/Nrf2 Signaling Pathway Inhibits Oxidative Damage and Improves Heart Failure in Rats
摘要
Abstract
Objective:To investigate the effects of miR-425-5p on heart failure in rats and preliminari-ly explore its potential mechanism of action.Methods:A rat model of heart failure was established through multiple intraperitoneal injections of doxorubicin hydrochloride.After successful modeling,healthy male SD rats were randomly divided into five groups:model group,NC-Inhibitor group,miR-425-5p Inhibitor group,NC-agomir group,and miR-425-5p agomir group,with 10 rats in each group.An additional 10 healthy SD rats were used as the control group.After 4 weeks of intervention,cardiac function indicators including left ventricular end-diastolic diameter(LVEDD),left ventricular end-systolic diameter(LVESD),left ventricu-lar ejection fraction(LVEF),and left ventricular fractional shortening(LVFS)were measured in each group.HE staining was used to observe morphological changes in myocardial tissue.The levels of malondialdehyde(MDA),superoxide dismutase(SOD),and glutathione peroxidase(GSH-Px)in myocardial tissue were de-termined by enzyme-linked immunosorbent assay(ELISA).Reactive oxygen species(ROS)levels in myo-cardial tissue were detected by flow cytometry.qRT-PCR was used to detect the levels of miR-425-5p,ERK,and Nrf2 mRNA in myocardial tissue.Western Blot was performed to detect the protein levels of p-ERK and Nrf2.Results:Compared with the control group,rats in the model group showed significantly in-creased LVEDD,LVESD,and MDA levels,while LVEF,LVFS,SOD,GSH-Px,and ROS levels were sig-nificantly decreased.Pathological damage to myocardial tissue was increased,and miR-425-5p mRNA levels were significantly reduced.Additionally,ERK mRNA,Nrf2 mRNA,p-ERK,and Nrf2 protein expression levels were significantly decreased.Compared with the model group,rats in the miR-425-5p Inhibitor group exhibited further increases in LVEDD,LVESD,and MDA levels,with decreases in LVEF,LVFS,SOD,GSH-Px,and ROS levels.Pathological damage to myocardial tissue was exacerbated,and ERK mRNA,Nrf2 mRNA,p-ERK,and Nrf2 protein expression levels were significantly reduced.In contrast,rats in the miR-425-5p agomir group showed significant decreases in LVEDD,LVESD,and MDA levels,with increases in LVEF,LVFS,SOD,GSH-Px,and ROS levels.Pathological damage to myocardial tissue was alleviated,and ERK mRNA,Nrf2 mRNA,p-ERK,and Nrf2 protein expression levels were significantly increased.Conclu-sion:miR-425-5p inhibits heart failure in rats by regulating oxidative damage mediated by the ERK/Nrf2 signaling pathway.关键词
心力衰竭/miR-425-5p/氧化损伤/ERK/Nrf2信号通路Key words
Heart failure/miR-425-5p/Oxidative damage/ERK/Nrf2 signaling pathway引用本文复制引用
牛素贞,白玉豪,牛琳,王孟彦,邓佳..miR-425-5p调控ERK/Nrf2信号通路介导的氧化损伤抑制大鼠心力衰竭[J].河北医学,2025,31(5):711-717,7.基金项目
河北省石家庄市科技计划项目,(编号:2412006403) （编号:2412006403）
