Article(id=1307269480451699257, tenantId=1146029695717560320, journalId=1302318977290174537, issueId=1307269479684133809, articleNumber=null, orderNo=null, doi=10.19664/j.cnki.1002-2392.260133, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1743350400000, receivedDateStr=2025-03-31, revisedDate=1764604800000, revisedDateStr=2025-12-02, acceptedDate=null, acceptedDateStr=null, onlineDate=1789606932031, onlineDateStr=2026-09-17, pubDate=1784476800000, pubDateStr=2026-07-20, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1789606932031, onlineIssueDateStr=2026-09-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1789606932031, creator=13701087609, updateTime=1789606932031, updator=13701087609, issue=Issue{id=1307269479684133809, tenantId=1146029695717560320, journalId=1302318977290174537, year='2026', volume='54', issue='7', pageStart='1', pageEnd='128', issueExtLink='null', onlineDate='null', pubDate='1784476800000', pubDateStr='2026-07-20', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1789606931849, creator='13701087609', updateTime=1789606931849, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=5, endPage=11, ext={EN=ArticleExt(id=1307269480611082810, articleId=1307269480451699257, tenantId=1146029695717560320, journalId=1302318977290174537, language=EN, title=Mechanism of Icaritin in Improving Myocardial Injury in Septic Mice via the AMPK/NLRP3 Pathway, columnId=null, journalTitle=Acta Chinese Medicine and Pharmacology, columnName=null, runingTitle=null, highlight=null, articleAbstract=
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.
, authors=Fengxiao SUN
1, Qingyan WANG
1, Jing ZHANG
1, Bo DONG
2, *, authorsList=Fengxiao SUN, Qingyan WANG, Jing ZHANG, Bo DONG, authorCompany=null, correspAuthors=Bo DONG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1307269481080844859, articleId=1307269480451699257, tenantId=1146029695717560320, journalId=1302318977290174537, language=CN, title=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, columnId=1303760926633652690, journalTitle=中医药学报, columnName=实验研究, runingTitle=null, highlight=null, articleAbstract=
目的: 探究淫羊藿素(ICT)对脓毒症心肌损伤的干预机制。
方法: 将小鼠随机分为对照组、模型组、AMPK激活剂组(MET组)、淫羊藿素组(ICT组)、淫羊藿素组+AMPK抑制剂化合物C组(ICT+CC组),每组12只。除对照组外,其余小鼠腹腔注射LPS造模。ICT组造模前30 min腹腔注射ICT,ICT+CC组同时注射AMPK抑制剂Compound C。造模24 h后,检测小鼠心功能、心肌病理变化、AMPK通路和焦亡相关蛋白表达及血清炎症因子和心肌损伤标志物浓度。
结果: ICT和AMPK激活剂的干预明显提高了脓毒症小鼠生存率,心脏LVEF、LVFS值升高(P < 0.05),LVIDD、LVIDS降低(P < 0.05);心肌组织损伤减轻,炎症细胞浸润减少;血清TNF-α、IL-1β、IL-18、CK-MB以及LDH水平降低(P < 0.05);蛋白p-AMPK/AMPK比值升高(P < 0.05),NLRP3、ASC、Cleaved Caspase-1、GSDMD-NT、Cleaved IL-1β表达减少(P < 0.05)。而Compound C可逆转ICT对心肌损伤的改善效果,炎症指标升高,焦亡蛋白表达增加。
结论: ICT可改善小鼠脓毒症心肌损伤和炎症反应,其作用机制可能与激活AMPK抑制NLRP3信号通路介导的细胞焦亡有关。
, authors=孙凤霄
1, 王磬妍
1, 张敬
1, 董波
2, *, authorsList=孙凤霄, 王磬妍, 张敬, 董波, authorCompany=null, correspAuthors=董波, authorNote=
孙凤霄(1999-),女,硕士研究生,从事中西医结合心系疾病相关研究。
, correspAuthorsNote=
* 董波(1964 -),男,博士,教授,从事中西医结合心系疾病相关研究。
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