Article(id=1291705006202311606, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.19.008, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1741190400000, receivedDateStr=2025-03-06, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896072196, onlineDateStr=2026-08-05, pubDate=1760630400000, pubDateStr=2025-10-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896072196, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896072196, creator=13701087609, updateTime=1785896072196, updator=13701087609, issue=Issue{id=1291704892859638107, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='19', pageStart='2701', pageEnd='2850', issueExtLink='null', onlineDate='null', pubDate='1760630400000', pubDateStr='2025-10-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896045171, creator='13701087609', updateTime=1785896787712, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708007352656266, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708007352656267, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704892859638107, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2741, endPage=2748, ext={EN=ArticleExt(id=1291705008022639543, articleId=1291705006202311606, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of bortezomib on oxidative stress and apoptosis in RSC96 cells, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the temporal association and molecular mechanism of bortezomib-induced mitochondrial oxidative stress and apoptosis in Schwann cells.
Methods Rat Schwann RSC96 cells were cultured in vitro and treated with different concentrations of bortezomib to establish an in vitro model of bortezomib damaged RSC96 cells. The assessment of cell viability was conducted by means of the CCK-8 method, and the morphological alterations observed in each group of cells were documented through inverted microscope analysis. DCFH-DA and Hoechst staining were combined with fluorescence microscopy to determine the content of reactive oxygen species. JC-1 staining was used to detect mitochondrial membrane potential level, and the degree of mitochondrial permeability transition pore opening and Ca2+ concentration were detected by fluorescence microscope. Annexin V-FITC/PI dual labeling was used to detect cell apoptosis. ELISA was used to detect the levels of inflammatory factors TNF-α, IL-1β, and IL-6.
Results In comparison with the control group, as the bortezomib concentration increased, the viability of RSC96 cells decreased in a concentration-dependent manner. The cell gap increased, the number of cells decreased significantly, the nucleus solidified, and the cells exhibited typical characteristics of apoptosis. Furthermore, bortezomib induced a reactive oxygen species burst in RSC96 cells in a dose-dependent manner, resulting in depolarization of mitochondrial membrane potential, cytosolic Ca2+ overload, continuous opening of the mitochondrial permeability transition pore, and a significant increase in the apoptosis rate of RSC96 cells.
Conclusion Bortezomib has been shown to induce programmed cell death apoptosis in Schwann cells by activating an axis involving oxidative stress, mitochondrial damage, and subsequent apoptosis. This finding suggests that oxidative stress and mitochondrial damage may represent pivotal mechanisms of bortezomib-induced toxicity, thus providing a novel target for the intervention of BIPN.
, authors=Quan ZHANG, Yan-qi SONG, Ai-di WANG, Lin MA, Bao-shan LIU, authorsList=Quan ZHANG, Yan-qi SONG, Ai-di WANG, Lin MA, Bao-shan LIU, authorCompany=null, correspAuthors=Bao-shan LIU, 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=1291705008496595896, articleId=1291705006202311606, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=硼替佐米诱导施万细胞氧化应激与线粒体依赖性凋亡的机制研究, 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 探究硼替佐米（BTZ）对施万细胞氧化应激、线粒体损伤和细胞凋亡的影响和机制。
方法 体外培养大鼠RSC96施万细胞，用不同浓度硼替佐米处理RSC96细胞，建立硼替佐米损伤的RSC96细胞神经毒性模型，CCK-8法检测细胞活力，用倒置显微镜观察各组细胞形态变化，用DCFH-DA和Hoechst染色法结合荧光显微镜检测荧光强度以确定细胞活性氧（ROS）产生水平，用JC-1荧光探针试剂盒检测线粒体膜电位（MMP），用荧光显微镜检测线粒体通透性转换孔开放程度（MPTP）与Ca2+浓度，用Annexin V-FITC/PI双标记法检测细胞凋亡水平，用ELISA法检测炎性因子TNF-α、IL-1β及IL-6含量。
结果 与正常RSC96细胞相比，不同浓度硼替佐米处理后，RSC96细胞存活率呈剂量依赖性降低，细胞间隙增大，数目明显减少，核固缩，细胞呈凋亡典型特征。硼替佐米剂量依赖性诱导RSC96细胞活性氧爆发，线粒体膜电位去极化，细胞Ca2+超载，线粒体通透性转换孔持续开放，RSC96细胞凋亡率显著升高。
结论 硼替佐米通过激活氧化应激-线粒体损伤-细胞凋亡轴（OMAA）触发施万细胞程序性死亡，氧化应激和线粒体损伤可能是硼替佐米引起细胞毒性的关键机制，为BIPN的靶向干预提供新靶点。
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张权（1998年-），男，硕士研究生，主要从事中西医结合血液与肿瘤疾病研究
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