Article(id=1314923099150189051, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922986466009203, articleNumber=null, orderNo=null, doi=null, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1753113600000, receivedDateStr=2025-07-22, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791431696926, onlineDateStr=2026-10-08, pubDate=1773936000000, pubDateStr=2026-03-20, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791431696926, onlineIssueDateStr=2026-10-08, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791431696926, creator=13701087609, updateTime=1791431696926, updator=13701087609, issue=Issue{id=1314922986466009203, tenantId=1146029695717560320, journalId=1234093305789726721, year='2026', volume='46', issue='3', pageStart='1185', pageEnd='1776', issueExtLink='null', onlineDate='null', pubDate='1773936000000', pubDateStr='2026-03-20', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1791431670061, creator='13701087609', updateTime=1791431955369, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1314924183251935526, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922986466009203, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1314924183251935527, tenantId=1146029695717560320, journalId=1234093305789726721, issueId=1314922986466009203, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1646, endPage=1654, ext={EN=ArticleExt(id=1314923099338932732, articleId=1314923099150189051, tenantId=1146029695717560320, journalId=1234093305789726721, language=EN, title=Protective effect of astaxanthin on the mitochondrial lesions induced by arsenic in HT-22 cells, columnId=1234106388687934088, journalTitle=China Environmental Science, columnName=Environmental Toxicology and Environmental Health, runingTitle=null, highlight=null, articleAbstract=

This study focused on the protective mechanism of astaxanthin (AST) against arsenic-induced mitochondrial-dependent apoptosis in mouse hippocampal neuronal cells (HT-22). An in vitro sodium arsenite (NaAsO₂) exposure model was established in HT-22cells, including control, NaAsO₂-exposed (4, 6, 8, 10μmol/L), AST-treated (2μmol/L), and AST-intervened (2μmol/L AST +10μmol/L NaAsO₂) groups, so as to evaluate the effects of AST intervention on arsenic-induced neural lesions. DCFH-DA was used to detect the level of reactive oxygen species (ROS). An ATP kit was used to assess the energy metabolism of mitochondria via ATP production. The levels of protein, including PGAM5 and signaling pathways of mitochondrial dynamics (fission/fusion), autophagy, and apoptosis, was analyzed by Western blot. Results showed that NaAsO₂ exposure significantly induced increased generation of ROS (P<0.05), decreased synthesis of ATP (P<0.05), activation of PGAM5, up-regulation of p-Drp1-Ser616, and down-regulation of p-Drp1-Ser637 and mitochondrial fusion proteins (OPA1, MFN1), leading to excessive mitochondrial fission. Intervention by AST effectively reversed these effects (P<0.05), which were demonstrated by the inhibition of PGAM5-mediated mitochondrial fission, alleviation of oxidative stress, and reversion of energy metabolism. It is supposed that AST plays a role in AMPK-mTOR-dependent autophagy and mitochondrial apoptosis. On one hand, AST inhibited AMPK phosphorylation which subsequently activated mTOR and down-regulated LC3II/LC3I ratio (autophagy marker); on the other hand, AST down-regulated pro-apoptotic proteins (Bax, cleaved-caspase-3), and upregulated anti-apoptotic Bcl-2 (P<0.05), thereby regulating AMPK-mTOR-dependent autophagy and mitochondrial apoptosis. This study suggests that AST protects against NaAsO₂-induced neurotoxicity by targeting PGAM5through the recovery of mitochondrial dynamics, improvement of energy metabolism, and regulation of AMPK-mTOR-autophagy-apoptosis axis, providing highlights on potential therapeutic strategies for arsenic-related neuronal damage.

, authors=Yao CHEN, Man YU, Ying-jie LIU, Yi-xin ZHANG, Hang REN, Mei WANG^*, authorsList=Yao CHEN, Man YU, Ying-jie LIU, Yi-xin ZHANG, Hang REN, Mei WANG, authorCompany=null, correspAuthors=Mei WANG, 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=1314923099645116925, articleId=1314923099150189051, tenantId=1146029695717560320, journalId=1234093305789726721, language=CN, title=虾青素对砷致HT-22细胞线粒体损伤的保护作用及机制, columnId=1234106394006311784, journalTitle=中国环境科学, columnName=环境毒理与健康, runingTitle=null, highlight=null, articleAbstract=

探究虾青素（AST）对环境污染物砷诱导小鼠海马神经元细胞（HT-22）线粒体途径依赖性凋亡的保护机制；通过建立HT-22细胞NaAsO₂暴露模型（0，4，6，8，10μmol/L）并设置虾青素（2μmol/L）单独处理组及虾青素干预组（2μmol/L AST + 10μmol/L NaAsO₂），评价虾青素对砷致神经细胞损伤的干预效果；利用二氯荧光素（DCFH-DA）检测活性氧（ROS）水平，ATP试剂盒评估线粒体能量代谢功能，并结合免疫印迹（Western blot）技术分析了PGAM5信号通路、线粒体动力学（分裂/融合）、自噬及凋亡关键蛋白的表达变化．结果表明，NaAsO₂暴露显著诱导HT-22细胞ROS过量生成（P<0.05），导致ATP合成减少（P<0.05），并激活PGAM5，促进Drp1-Ser616磷酸化，抑制Drp1-Ser637磷酸化及融合蛋白（OPA1, MFN1）表达，引发线粒体过度分裂．虾青素干预可有效逆转上述损伤（P<0.05），显著抑制PGAM5介导的线粒体分裂，减轻氧化应激并改善能量代谢障碍．机制上，虾青素通过抑制AMPK磷酸化并恢复mTOR活性，降低自噬标志蛋白LC3II/LC3I比值，同时下调促凋亡蛋白（Bax, cleaved-caspase-3）表达并上调抗凋亡蛋白Bcl-2（P<0.05），进而调控AMPK-mTOR通路依赖性自噬与线粒体凋亡途径．本研究表明，虾青素通过靶向PGAM5调控线粒体动力学平衡，改善能量代谢，并干预AMPK-mTOR-自噬-凋亡信号级联反应，对NaAsO₂诱导的神经细胞线粒体途径依赖性凋亡发挥关键保护作用．

, authors=陈峣, 于漫, 刘映洁, 张艺馨, 任航, 王梅^*, authorsList=陈峣, 于漫, 刘映洁, 张艺馨, 任航, 王梅, authorCompany=null, correspAuthors=王梅, authorNote=, correspAuthorsNote=, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=U4Ss/5Q3YCcBGfwHhMhLZw==, magXml=mRv0lefcSE2EG1hwfgEhUg==, pdfUrl=null, pdf=jbk3Y/QkBZBfbFpBnQFYIg==, pdfFileSize=2367751, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=pOnm22D2uZlXsSnywuvIAQ==, mapNumber=null, fund=null)}, authors=[Author(id=1314923100232319490, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314923099150189051, orderNo=0, firstName=null, middleName=null, lastName=null, nameCn=null, orcid=null, stid=null, country=null, authorPic=null, dead=0, email=532293903@qq.com, emailSecond=null, emailThird=null, correspondingAuthor=0, authorType=1, ext={EN=AuthorExt(id=1314923100429451780, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314923099150189051, authorId=1314923100232319490, language=EN, stringName=Yao CHEN, firstName=Yao, middleName=null, lastName=CHEN, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=School of Basic Medicine, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1314923100488172037, tenantId=1146029695717560320, journalId=1234093305789726721, articleId=1314923099150189051, authorId=1314923100232319490, language=CN, stringName=陈峣, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=null, address=辽宁中医药大学基础医学院，辽宁 沈阳 110847, bio={"content":"

陈峣（1991-），女，吉林通化人，讲师，博士，研究方向为环境毒物神经损伤机制研究．发表论文4篇．532293903@qq.com.

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陈峣（1991-），女，吉林通化人，讲师，博士，研究方向为环境毒物神经损伤机制研究．发表论文4篇．532293903@qq.com.

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