陕西医学杂志2026，Vol.55Issue(1)：29-34,6.DOI:10.3969/j.issn.1000-7377.2026.01.005
内皮祖细胞微囊泡通过p38丝裂原活化蛋白激酶/核因子-κB通路保护心肌缺血再灌注损伤实验研究
Experimental study of endothelial progenitor cell-derived microvesicles protect myocardial ischemia-reperfusion injury through the p38 MAPK/NF-κB pathway
摘要
Abstract
Objective:To investigate the cardioprotective effects of endothelial progenitor cell-derived microvesi-cles(EPC-MVs)against myocardial ischemia-reperfusion injury(MIRI).Methods:Endothelial progenitor cells(EPCs)were isolated and cultured using density gradient centrifugation combined with differential adhesion meth-ods.EPC-MVs were collected via ultracentrifugation.Sprague-Dawley rats were randomized into three groups(n=3 per group):sham-operated,MIRI,and EPC-MVs-treated.Cardiac function was assessed by transthoracic echocardio-graphy to measure left ventricular end-systolic diameter(LVESD),end-diastolic diameter(LVEDD),ejection frac-tion(EF),and fractional shortening(FS).Serum levels of lactate dehydrogenase(LDH),creatine kinase-MB(CK-MB),cardiac troponin I(cTnI),tumor necrosis factor-α(TNF-α),and interleukin-1β(IL-1β)were quantified by enzyme-linked immunosorbent assay(ELISA).Histopathological alterations in myocardial tissue were evaluated via hema-toxylin-eosin(HE)staining.Protein expression levels of phosphorylated p38 mitogen-activated protein kinase(p-p38 MAPK)and nuclear factor-kappa B(p-NF-κB)were analyzed by Western blot.Results:Compared to the MIRI group,the EPC-MVs group exhibited significantly reduced LVESD and LVEDD(all P＜0.05),accompanied by in-creased EF and FS(all P＜0.05).Serum biomarkers of myocardial injury(LDH,CK-MB,cTnI)and pro-inflamma-tory cytokines(TNF-α,IL-1β)were markedly attenuated in the EPC-MVs group(all P＜0.05).Histopathological analysis revealed improved myocardial architecture in the EPC-MVs group,characterized by alleviated myofibril dis-array,reduced interstitial inflammatory cell infiltration,and diminished necrosis compared to the MIRI group.West-ern blot demonstrated that EPC-MVs treatment significantly suppressed MIRI-induced activation of p-p38 MAPK and p-NF-κB(all P＜0.01).Conclusion:EPC-MVs confer cardioprotection against MIRI,potentially through inhibi-tion of the p38 MAPK/NF-κB signaling pathway,thereby attenuating inflammatory cascades.关键词
心肌缺血再灌注损伤/内皮祖细胞微囊泡/细胞通路/炎症/心肌保护/信号转导Key words
Myocardial ischemia-reperfusion injury/Endothelial progenitor cell microvesicles/Cellular path-ways/Inflammation/Cardioprotection/Signal transduction分类
医药卫生引用本文复制引用
宋艳玲,陈明慧,刘皇军..内皮祖细胞微囊泡通过p38丝裂原活化蛋白激酶/核因子-κB通路保护心肌缺血再灌注损伤实验研究[J].陕西医学杂志,2026,55(1):29-34,6.基金项目
海南省自然科学基金资助项目(823RC577) （823RC577）
