Article(id=1317125429366997681, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.03.017, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791956773368, onlineDateStr=2026-10-14, pubDate=1773072000000, pubDateStr=2026-03-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791956773368, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791956773368, creator=13701087609, updateTime=1791956773368, updator=13701087609, issue=Issue{id=1317125400581485316, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='3', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1773072000000', pubDateStr='2026-03-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791956766504, creator='13701087609', updateTime=1791958763799, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133777898418844, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133777898418845, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125400581485316, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=89, endPage=92, ext={EN=ArticleExt(id=1317125429702542002, articleId=1317125429366997681, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Formononetin Inhibits Ferroptosis Induced by Oxygen Glucose Deprivation/Reoxygenation in HT22 Cells by Activating Nrf2/GPX4 Pathway, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To reveal whether Formononetin(FMN)inhibits ferroptosis in HT22 cells induced by oxygen glucose deprivation/reoxygenation by activating the nuclear factor erythroid 2-related factor 2(Nrf2)/Glutathione peroxidase 4(GPX4)?pathway.
Methods HT22 cells were subjected to oxygen-glucose deprivation/reoxygenation(OGD/R)damage to create an in vitro model, and HT22 cells were divided into control group(CON), FMN group(FMN), model group(OGD/R), model + FMN group(OGD/R + FMN), model + ML385 group(OGD/R + ML385), model + RSL3 group(OGD/R + RSL3). The CCK-8 method was used to detect the cell viability. DCFH-DA probe was used to detect the level of intracellular ROS. TUNEL staining and flow cytometry were used to detect the apoptosis. The colorimetric method was used to detect Fe2+ content in cells. Western blot was used to detect the protein expression levels of Nrf2 and GPX4.
Results Compared with those in the CON group, the cell proliferation activity in the OGD/R group was significantly reduced, the Fe2+ content, ROS level and apoptosis ratio were significantly increased, and the protein expressions of Nrf2 and GPX4 were significantly decreased(P > 0.05). Compared with the OGD/R group, the OGD/R + FMN group had significantly increased cell proliferation activity(P < 0.05), Fe2+ content, ROS level and apoptosis ratio significantly decreased and the expressions of Nrf2 and GPX4 proteins increased significantly. Compared with those of the OGD/R group, the cell proliferative activity of the OGD/R + ML385 group and the OGD/R + RSL3 group was significantly decreased(P < 0.05), the Fe2+ content, ROS level and apoptosis ratio were significantly increased, the expression of Nrf2 protein in the OGD/R + ML835 group was significantly decreased(P < 0.05), and the expression of GPX4 protein in the OGD/R + RSL3 group was significantly decreased(P < 0.05).
Conclusion FMN may inhibit ferroptosis induced by oxygen glucose deprivation/reoxygenation by activating the Nrf2/GPX4 pathway.
, authors=Liang CHEN
1, Mei TANG
2, Wenxiu WANG
2, Min ZHANG
2, Liping CAO
2, Qiansong HE
1, 2, authorsList=Liang CHEN, Mei TANG, Wenxiu WANG, Min ZHANG, Liping CAO, Qiansong HE, authorCompany=null, correspAuthors=Qiansong HE, 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=1317125430105195187, articleId=1317125429366997681, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=芒柄花素通过激活Nrf2/GPX4通路抑制氧糖剥夺/复氧诱导的HT22细胞铁死亡, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 旨在揭示芒柄花素(Formononetin,FMN)是否通过激活Nrf2/GPX4通路抑制氧糖剥夺/复氧诱导的HT22细胞发生铁死亡。
方法 构建HT22细胞氧-糖剥夺/再氧合(Oxygen-glucose deprivation/reoxygenation,OGD/R)损伤模型,将HT22细胞分为空白对照组(CON)、芒柄花素组(FMN)、模型组(OGD/R)、模型+芒柄花素组(OGD/R + FMN)、模型+ ML385(Nrf2抑制剂)组(OGD/R + ML385)、模型+ RSL3(GPX4抑制剂)组(OGD/R + RSL3);采用CCK-8法检测细胞活力;DCFH-DA探针检测细胞内ROS水平;TUNEL染色和流式细胞仪检测细胞凋亡;比色法检测细胞内Fe2+含量;Western blot检测Nrf2和GPX4的蛋白表达水平。
结果 与CON组相比,OGD/R组中细胞增殖活性显著降低,Fe2+含量、ROS水平和细胞凋亡比例显著增高,Nrf2和GPX4的蛋白表达显著降低(P > 0.05);与OGD/R组相比,OGD/R + FMN组细胞增殖活性显著增加(P < 0.05),Fe2+含量、ROS水平和细胞凋亡比例显著下降,Nrf2和GPX4蛋白表达量显著上升;与OGD/R组相比,OGD/R + ML385组和 OGD/R + RSL3组的细胞增殖活性均显著降低(P < 0.05),Fe2+含量、ROS水平和细胞凋亡比例显著上升,OGD/R + ML835组中 Nrf2蛋白表达量显著降低(P < 0.05),OGD/R + RSL3组中GPX4蛋白表达量显著降低(P < 0.05)。
结论 芒柄花素可能通过激活Nrf2/GPX4通路抑制氧糖剥夺/复氧诱导的HT22细胞铁死亡。
, authors=陈靓
1, 唐梅
2, 王文秀
2, 张敏
2, 曹丽平
2, 何前松
1, 2, authorsList=陈靓, 唐梅, 王文秀, 张敏, 曹丽平, 何前松, authorCompany=null, correspAuthors=何前松, authorNote=
陈靓(1999 -),女,重庆人,硕士在读,研究方向:中医药防治脑血管疾病。
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何前松(1979 -),男(仡佬族),贵州道真人,教授,博士研究生导师,博士,研究方向:中医药防治脑血管疾病。E-mail:
hqs0820@126.com。
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