中医药学报2026，Vol.54Issue(7)：5-11,7.DOI:10.19664/j.cnki.1002-2392.260133
淫羊藿素通过AMPK/NLRP3通路改善脓毒症小鼠心肌损伤的机制研究
Mechanism of Icaritin in Improving Myocardial Injury in Septic Mice via the AMPK/NLRP3 Pathway
摘要
Abstract
Objective:To explore the intervention mechanism of icaritin(ICT)on myocardial injury in sepsis.Methods:Mice were divided into control group,model group,AMPK activator(MET)group,icaritin(ICT)group and icaritin+AMPK inhibitor compound C(ICT+CC)group,with 12 mice in each group.Except for the control group,the other mice were intraperitoneally injected with LPS.ICT group was intraperitoneally injected with ICT 30 minutes before modeling,and ICT+CC group was injected with AMPK inhibitor Compound C at the same time.After 24 hours of modeling,cardiac function,myocardial pathological changes,AMPK pathway and pyroptosis-related protein expression,serum inflammatory factors and myocardial injury markers were detected.Results:The intervention of ICT and AMPK activators significantly improved the survival rate of mice,increased cardiac LVEF and LVFS,and decreased LVIDD and LVIDS.Tissue damage was reduced and inflammatory cell infiltration was reduced.The levels of serum TNF-α,IL-1β,IL-18,CK-MB and LDH were decreased.The ratio of p-AMPK/AMPK was increased,and the expression of NLRP3,ASC,Cleaved Caspase-1,GSDMD-NT and Cleaved IL-1β was decreased(P<0.05).Compound C could reverse the improvement effect of ICT on myocardial injury,increase inflammation index and pyroptosis protein expression(P<0.05).Conclusion:ICT can improve myocardial injury and inflammatory response in sepsis mice,and its mechanism may be related to the activation of AMPK to inhibit pyroptosis mediated by NLRP3 signaling pathway.关键词
淫羊藿素/脓毒症/心肌损伤/细胞焦亡/AMPK/NLRP3通路Key words
Icaritin/Sepsis/Myocardial injury/Pyroptosis/AMPK/NLRP3 pathway分类
医药卫生引用本文复制引用
孙凤霄,王磬妍,张敬,董波..淫羊藿素通过AMPK/NLRP3通路改善脓毒症小鼠心肌损伤的机制研究[J].中医药学报,2026,54(7):5-11,7.基金项目
国家自然科学基金面上项目(82070382) （82070382）
山东省泰山学者基金项目(ts20190979) （ts20190979）
