Article(id=1276976171510272575, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251021.901, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1755100800000, receivedDateStr=2025-08-14, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384444357, onlineDateStr=2026-06-25, pubDate=1768406400000, pubDateStr=2026-01-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384444357, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384444357, creator=13701087609, updateTime=1782384444357, updator=13701087609, issue=Issue{id=1276976057215488893, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='2', pageStart='301', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1768406400000', pubDateStr='2026-01-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1782384417107, creator='13701087609', updateTime=1782384524478, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976507658563977, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976507658563978, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276976057215488893, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=553, endPage=564, ext={EN=ArticleExt(id=1276976171711599169, articleId=1276976171510272575, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Naotaifang alleviates cerebral ischemia-reperfusion injury by inhibiting neuronal ferroptosis and pyroptosis through Nrf2 regulation, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study aims to investigate the effects of Naotaifang (NTF) on neuronal ferroptosis and pyroptosis in cerebral ischemia-reperfusion injury (CIRI), with a focus on nuclear factor erythroid 2-related factor 2 (Nrf2). A rat model of CIRI was established by middle cerebral artery occlusion/reperfusion (MCAO/R). Sprague-Dawley rats were randomly assigned to a sham group, a model group, low/medium/high-dose (4.5, 9, 18 g·kg^-1, respectively) NTF groups, and a butylphthalide (60 mg·kg^-1) group (n=15 per group). After modeling, the treatment groups received corresponding agents by gavage once daily for 7 days, and the sham and model groups received an equal volume of normal saline. After treatment, the neurological function was assessed based on the Zea-Longa score, the infarct volume by TTC staining, and cellular morphology by HE staining. The levels of Fe²⁺, interleukin-1β (IL-1β), and interleukin-18 (IL-18) were measured by ELISA, and those of malondialdehyde (MDA) and glutathione (GSH) by biochemical assays. Western blot was employed to examine the expression levels of Nrf2, glutathione peroxidase 4 (GPX4), NOD-like receptor family pyrin domain-containing 3 (NLRP3), and the N-terminal fragment of gasdermin D (GSDMD-N). In the cell experiment, oxygen-glucose deprivation/reperfusion (OGD/R) was used to model CIRI in SH-SY5Y cells. siRNA-mediated Nrf2 knockdown (si-Nrf2) was employed to probe into the role of Nrf2 in OGD/R-induced ferroptosis and pyroptosis and the intervention effect of NTF. Membrane damage was evaluated by Hoechst/propidium iodide staining and LDH release, and GPX4 and GSDMD immunofluorescence was employed to indicate ferroptosis and pyroptosis, respectively. Fe²⁺, MDA, and GSH were quantified biochemically, and the levels of IL-1β and IL-18 by ELISA. The expression of Nrf2, GPX4, NLRP3, and GSDMD-N was quantified by Western blot. The cellular ultrastructure was observed by transmission electron microscopy. The results of the animal experiment showed that NTF promoted the expression of Nrf2 to alleviate neuronal ferroptosis and pyroptosis, thus producing significant neuroprotection against CIRI in a dose-dependent manner. The results of the cell experiment showed that the neuroprotective effects of NTF after CIRI were mediated by Nrf2-dependent suppression of neuronal ferroptosis and pyroptosis. Taken together, NTF attenuates CIRI by suppressing neuronal ferroptosis and pyroptosis through Nrf2-mediated regulation.

, authors=null, authorsList=Wen-feng WANG, Jun LIAO, Xiu-li ZHANG, Hui-fang NIE, Tong YANG, Xin-ai LIU, Zhi-gang MEI, Jin-wen GE, authorCompany=null, correspAuthors=Zhi-gang MEI, Jin-wen GE, 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=1276976172080697923, articleId=1276976171510272575, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=脑泰方通过Nrf2调控抑制神经元铁死亡与焦亡减轻脑缺血再灌注损伤, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

基于核因子E2相关因子2 （nuclear factor erythroid 2-related factor 2, Nrf2）探讨脑泰方（Naotaifang, NTF）对脑缺血再灌注损伤（cerebral ischemia-reperfusion injury, CIRI）神经元铁死亡和焦亡的影响。体内采用大脑中动脉栓塞／再灌注（middle cerebral artery occlusion/reperfusion, MCAO/R）方法建立大鼠CIRI模型。SD大鼠随机分为假手术组，模型组，脑泰方低、中、高剂量组（4.5、9、18 g·kg^-1）及丁苯酞组（60 mg·kg^-1），每组15只。造模完成后，各治疗组连续灌胃7 d，每天1次，假手术组及模型组给子同体积生理盐水灌胃。治疗完成后，采用Zea Longa法进行神经功能评分；TTC染色检测脑梗死体积；HE染色观察细胞形态；ELISA检测Fe²⁺，白细胞介素-1β（interleukin 1β，IL-1β）及白细胞介素-18（interleukin 18, IL-18）水平，生化检测丙二醛（malondialdehyde, MDA）及谷胱甘肽（glutathione, GSH）含量；Western blot检测Nrf2、谷胱甘肽过氧化酶4 （glutathione peroxidase 4, GPX4）、NOD样受体热蛋白结构域蛋白3（NOD-like receptor thermal protein domain associated protein 3, NLRP3）及Gasdermin D蛋白N端片段（GSDMD-N）的表达。体外采用氧-糖剥夺／再灌注（oxygen-glucose deprivation/reperfusion, OGD/R）诱导SH-SY5Y细胞模拟CIRI体外细胞模型，运用si-Nrf2转染技术探讨Nrf2对OGD/R细胞铁死亡和焦亡的影响及NTF的干预作用。Hoechst/PI荧光染色及LDH释放试验检测细胞膜的损伤程度；GPX4及GSDMD荧光染色检测细胞铁死亡及焦亡；生化检测Fe²⁺、MDA、GSH含量；ELISA检测IL-1β、IL-18炎症因子水平；Western blot检测Nrf2、GPX4、NLRP3及GSDMD-N铁死亡及焦亡相关蛋白表达；透射电镜观察细胞超微结构。结果表明，NTF通过促进Nrf2的表达，减轻神经元铁死亡和焦亡，对CIRI产生明显的神经保护作用，且NTF的保护作用呈剂量依赖性；NTF通过Nrf2调控抑制神经元铁死亡和焦亡，发挥CIRI后神经保护作用。综上所述，NTF可通过Nrf2调控抑制神经元铁死亡与焦亡，减轻脑缺血再灌注损伤。

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