Zou Ying-Hua, Zhou En, Xie Chen-Long, Sun Long, Zhang Yu-Jiao, Wang Chun-Chun, Li Xing, Guo Jun
Department of Anesthesiology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Department of Cardiovascular Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200000, China.
Open Med (Wars). 2025 Aug 19;20(1):20251255. doi: 10.1515/med-2025-1255. eCollection 2025.
This study aims to investigate the potential of electroacupuncture to mitigate myocardial ischemia-reperfusion injury (MIRI) by influencing N6-methyladenosine (m6A) methylation through modulation of the fat mass and obesity-associated protein (FTO).
An experimental murine model of MIRI was established by surgically occluding the left anterior descending coronary artery, followed by reperfusion. Electroacupuncture treatment targeting Neiguan acupoints was administered 7 days before ischemia induction. Cardiac function was evaluated using echocardiography, and myocardial infarction size was assessed through Evans Blue and triphenyltetrazolium chloride dual staining. To measure m6A methylation and mRNA expression of FTO and mediator complex subunit 1 (Med1), RNA immunoprecipitation and quantitative polymerase chain reaction were utilized. Western blot analysis was conducted to determine the protein expression levels of Med1, Bcl-2, and Bax.
Electroacupuncture pretreatment was associated with a reduction in myocardial injury, demonstrated by preserved ejection fraction and reduced infarct size. Enhanced FTO expression and decreased m6A methylation were observed in myocardial tissue following electroacupuncture treatment. Additionally, Med1 - a downstream target of m6A - exhibited decreased mRNA expression in the electroacupuncture-treated group, correlating with reduced cardiomyocyte apoptosis.
Electroacupuncture pretreatment may confer cardioprotective effects in MIRI by upregulating FTO, thereby modulating m6A methylation and reducing Med1 expression.
本研究旨在探讨电针通过调节脂肪量和肥胖相关蛋白（FTO）影响N6-甲基腺苷（m6A）甲基化来减轻心肌缺血再灌注损伤（MIRI）的潜力。
通过手术阻断左冠状动脉前降支建立MIRI实验小鼠模型，随后进行再灌注。在缺血诱导前7天给予针对内关穴的电针治疗。使用超声心动图评估心脏功能，并通过伊文思蓝和氯化三苯基四氮唑双重染色评估心肌梗死面积。为了测量FTO和中介体复合物亚基1（Med1）的m6A甲基化和mRNA表达，采用了RNA免疫沉淀和定量聚合酶链反应。进行蛋白质印迹分析以确定Med1、Bcl-2和Bax的蛋白质表达水平。
电针预处理与心肌损伤减轻相关，表现为射血分数保留和梗死面积减小。电针治疗后心肌组织中FTO表达增强，m6A甲基化降低。此外，m6A的下游靶点Med1在电针治疗组中mRNA表达降低，与心肌细胞凋亡减少相关。
电针预处理可能通过上调FTO，从而调节m6A甲基化并降低Med1表达，对MIRI发挥心脏保护作用。
