Article(id=1292130441612513347, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.07.011, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1773590400000, receivedDateStr=2026-03-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785997503902, onlineDateStr=2026-08-06, pubDate=1776355200000, pubDateStr=2026-04-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785997503902, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785997503902, creator=13701087609, updateTime=1785997503902, updator=13701087609, issue=Issue{id=1292130366320562708, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='7', pageStart='901', pageEnd='1050', issueExtLink='null', onlineDate='null', pubDate='1776355200000', pubDateStr='2026-04-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785997485952, creator='13701087609', updateTime=1786014433453, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201449350516861, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201449350516862, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292130366320562708, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=968, endPage=974, ext={EN=ArticleExt(id=1292130441943863364, articleId=1292130441612513347, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of kaempferol improves rat skin flap ischemia-reperfusion injury by regulating GPX4 mediated iron death and NLRP3/Caspase-1/GSDMD pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the protective effect and underlying mechanism of kaempferol (Kae) on flap ischemia-reperfusion injury (FIRI) in rats by regulating glutathione peroxidase 4 (GPX4)-mediated ferroptosis and gasdermin D (GSDMD)-mediated pyroptosis.
Methods McFarlane method was used to establish the ischemia-reperfusion model of rat dorsal flap. A total of 91 SPF SD rats were randomly divided into sham group, model group, experimental group, agonist group, inhibitor group, Kae+agonist group and Kae+inhibitor group, with 13 rats in each group. After successful modeling, the experimental group was given kaempferol 50 mg·kg-1 by gavage; the agonist group was intraperitoneally injected with 2 mg·kg-1 NOD like receptor thermoprotein domain associated protein 3 (NLRP3) activator once a week; the inhibitor group was intraperitoneally injected with 30 mg·kg-1 disulfiram once a week; the Kae+agonist group received intraperitoneal injection of 2 mg·kg-1 NLRP3 activator+50 mg·kg-1 kaempferol; the Kae+inhibitor group received intraperitoneal injection of 30 mg·kg-1 disulfiram+50 mg·kg-1 kaempferol for 2 weeks. The iron content in tissues was detected by iron content detection kit; the levels of serum interleukin-1 β (IL-1 β) and IL-18 were detected by enzyme linked immunosorbent assay (ELISA); the expressions of proliferating cell nuclear antigen (Ki67) and platelet endothelial cell adhesion molecule-1 (CD31) were detected by immunohistochemistry; the protein expressions of GPX4, Caspase-1 and GSDMD-NT were detected by Western blot.
Results The flap survival rates of the sham group, model group, experimental group, agonist group, inhibitor group, Kae+agonist group and Kae+inhibitor group were (96.73±1.10)%, (67.04±1.60)%, (85.39±1.22)%, (57.96±1.52)%, (75.80±1.72)%, (80.28±0.95)% and (90.49±0.76)%, respectively; the tissue iron content levels were (11.57±4.89), (68.04±7.64), (43.87±9.13), (85.97±8.41), (47.78±11.11), (69.68±6.17) and (29.36±7.66) μmol·L-1; the levels of IL-1 β were (43.83±13.96), (246.02±37.60), (172.19±29.46), (354.39±36.05), (153.56±26.89), (271.13±39.54) and (97.53±24.67) pg·mL-1, respectively; the relative expression levels of CD31 were 6 694.96±711.29, 2 126.32±277.21, 3 592.33±317.33, 484.36±56.24, 3 568.83±316.65, 1 901.66±383.85 and 4 804.18±360.03, respectively; the relative expression levels of Ki67 were 75.56±6.57, 24.11±4.02, 37.94±4.08, 12.17±2.28, 38.01±3.80, 24.32±2.76 and 54.65±7.01, respectively; the relative expression levels of GPX4 were 0.92±0.02, 0.30±0.07, 0.47±0.08, 0.12±0.04, 0.47±0.08, 0.27±0.07 and 0.62±0.13, respectively; the relative expression levels of Caspase-1 were 0.08±0.03, 0.40±0.07, 0.29±0.04, 0.68±0.07, 0.28±0.03, 0.40±0.06 and 0.18±0.06, respectively; the relative expression levels of GSDMD were 0.06±0.04, 0.57±0.05, 0.30±0.04, 0.93±0.09, 0.30±0.03, 0.56±0.07 and 0.16±0.02 respectively. There were statistically significant differences in the above indexes between model group and sham group, between experimental group and model group, and between Kae+agonist group, Kae+inhibitor group and experimental group (all P<0.05).
Conclusion Kaempferol can alleviate flap ischemia-reperfusion injury in rats, and its protective effect may be related to upregulating GPX4 expression, inhibiting ferroptosis, and regulating the NLRP3/Caspase-1/GSDMD pyroptosis signaling pathway.
, authors=Tao LIU, Zhen-xing JIANG, Zhi-jun HE, Yan LI, Wen CHEN, Jin-peng LI, Fei LI, Xiao-tao WEI, Bi-hui BAI, Yu-biao GU, authorsList=Tao LIU, Zhen-xing JIANG, Zhi-jun HE, Yan LI, Wen CHEN, Jin-peng LI, Fei LI, Xiao-tao WEI, Bi-hui BAI, Yu-biao GU, authorCompany=null, correspAuthors=Zhen-xing JIANG, 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=1292130442363293765, articleId=1292130441612513347, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=山奈酚通过调控GPX4介导的铁死亡及NLRP3/Caspase-1/GSDMD改善大鼠皮瓣缺血再灌注损伤的机制研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨山奈酚（Kae）通过调控谷胱甘肽过氧化物酶4（GPX4）介导的铁死亡及消皮素D（GSDMD）介导的细胞焦亡，对大鼠皮瓣缺血再灌注损伤（FIRI）的保护作用及其机制。
方法 用McFarlane法建立大鼠背部皮瓣缺血再灌注模型。将91只SPF级SD大鼠随机分为假手术组、模型组、实验组、激动剂组、抑制剂组、联合激动剂组和联合抑制剂组，每组13只。造模成功后，试验组按50 mg·kg-1山奈酚灌胃给药；激动剂组腹腔注射2 mg·kg-1 NOD样受体热蛋白结构域相关蛋白3（NLRP3）激活剂，每周1次；抑制剂组腹腔注射30 mg·kg-1双硫仑，每周1次；联合激动剂组腹腔注射2 mg·kg-1 NLRP3激活剂+50 mg·kg-1山奈酚；联合抑制剂组腹腔注射30 mg·kg-1双硫仑+50 mg·kg-1山奈酚，连续干预2 w。观察皮瓣存活情况；用铁含量检测试剂盒检测组织铁含量；用酶联免疫吸附试验（ELISA）法检测血清白细胞介素-1β（IL-1β）和IL-18水平；用免疫组化法检测增殖细胞核抗原（Ki67）和血小板内皮细胞黏附分子1（CD31）表达；用蛋白质印迹法检测GPX4、半胱氨酸天冬氨酸蛋白酶1（Caspase-1）和消皮素D-N-端结构域（GSDMD-NT）蛋白表达。
结果 假手术组、模型组、实验组、激动剂组、抑制剂组、联合激动剂组和联合抑制剂组的皮瓣存活率分别为（96.73±1.10）%、（67.04±1.60）%、（85.39±1.22）%、（57.96±1.52）%、（75.80±1.72）%、（80.28±0.95）%和（90.49±0.76）%，组织铁含量分别为（11.57±4.89）、（68.04±7.64）、（43.87±9.13）、（85.97±8.41）、（47.78±11.11）、（69.68±6.17）和（29.36±7.66）μmol·L-1，IL-1β水平分别为（43.83±13.96）、（246.02±37.60）、（172.19±29.46）、（354.39±36.05）、（153.56±26.89）、（271.13±39.54）和（97.53±24.67）pg·mL-1，CD31相对表达水平分别为6 694.96±711.29、2 126.32±277.21、3 592.33±317.33、484.36±56.24、3 568.83±316.65、1 901.66±383.85和4 804.18±360.03，Ki67相对表达水平分别为75.56±6.57、24.11±4.02、37.94±4.08、12.17±2.28、38.01±3.80、24.32±2.76和54.65±7.01，GPX4相对表达水平分别为0.92±0.02、0.30±0.07、0.47±0.08、0.12±0.04、0.47±0.08、0.27±0.07和0.62±0.13，Caspase1相对表达水平分别为0.08±0.03、0.40±0.07、0.29±0.04、0.68±0.07、0.28±0.03、0.40±0.06和0.18±0.06，GSDMD相对表达水平分别为0.06±0.04、0.57±0.05、0.30±0.04、0.93±0.09、0.30±0.03、0.56±0.07和0.16±0.02，模型组与假手术组比较、实验组与模型组比较、联合激动剂组和联合抑制剂组与实验组比较，上述指标在统计学上差异均有统计学意义（均P<0.05）。
结论 山奈酚可减轻大鼠皮瓣缺血再灌注损伤，其作用可能与上调GPX4表达、抑制铁死亡及调控NLRP3/Caspase-1/GSDMD焦亡通路有关。
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