中国临床医学2025，Vol.32Issue(3)：403-409,7.DOI:10.12025/j.issn.1008-6358.2025.20250279
运动后分泌代谢物3对心肌细胞缺血再灌注损伤的保护作用
Protective effect of exercise induced metabolite-3 in ischemia-reperfusion injury
摘要
Abstract
Objective To explore the protective effect of exercise-induced metabolite-3(EIM-3)on myocardial ischemia-reperfusion(I/R)injury and explore its underlying molecular mechanisms.Methods The physicochemical properties and half-life of EIM-3 were analyzed using the Human Metabolome Database(HMDB,https://hmdb.ca/).A primary rat cardiomyocyte hypoxia/reoxygenation(H/R)injury model was established.Cell apoptosis and viability were assessed using TUNEL assay and cell counting kit-8,respectively.Lactate dehydrogenase(LDH)levels in the cell culture supernatant were measured.Intracellular reactive oxygen species(ROS)levels were detected.Transcriptomic analysis was performed to identify potential signaling pathways and targets of EIM-3.Results Plasma levels of EIM-3 were elevated post-exercise.EIM-3 was characterized as a phospholipid small-molecule compound with a partition coefficient(logP)of 5.58 and a solubility(logS)of-7.6,indicating favorable lipophilicity and cell membrane permeability.In cardiomyocytes H/R injury modles,EIM-3 significantly inhibited apoptosis,increased cell viability,reduced intracellular ROS levels,and decreased LDH release(P＜0.01).Transcriptomic analysis suggested that EIM-3 exerts its protective function potentially by regulating glucose metabolim.Quantitative real-time polymerase chain reaction results confirmed that EIM-3 significantly upregulated the transcriptional level of pyruvate kinase M2(PKM2)in a dose-dependent manner(P＜0.001).Conclusions EIM-3 protects cardiomyocytes against I/R injury by modulating glucose metabolim.This study provides foundational insights into the mechanisms underlying exercise-induced cardioprotection.关键词
心肌梗死/缺血再灌注损伤/代谢组学Key words
myocardial infarction/ischemia-reperfusion injury/metabolomics分类
临床医学引用本文复制引用
程子杰,汪雪君,王子牧,钱菊英..运动后分泌代谢物3对心肌细胞缺血再灌注损伤的保护作用[J].中国临床医学,2025,32(3):403-409,7.基金项目
国家自然科学基金(82200288),中国博士后科学基金特别资助(2024T170158),中国博士后科学基金面上项目(2022M710755),复旦大学附属中山医院"卓越医师"临床博士后项目.Supported by National Natural Science Foundation of China(82200288),China Postdoctoral Science Foundation-Special Funding Program(2024T170158),China Postdoctoral Science Foundation-General Funding Program(2022M710755),and Outstanding Resident Clinical Postdoctoral Program of Zhongshan Hospital,Fudan University. （82200288）
