Article(id=1309635221826404613, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309635220643607372, articleNumber=null, orderNo=null, doi=10.12048/j.issn.1674-229X.2026.02.002, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746460800000, receivedDateStr=2025-05-06, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1790170968728, onlineDateStr=2026-09-23, pubDate=1771948800000, pubDateStr=2026-02-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1790170968728, onlineIssueDateStr=2026-09-23, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1790170968728, creator=13701087609, updateTime=1790170968728, updator=13701087609, issue=Issue{id=1309635220643607372, tenantId=1146029695717560320, journalId=1227999776411738115, year='2026', volume='36', issue='2', pageStart='81', pageEnd='160', issueExtLink='null', onlineDate='null', pubDate='1771948800000', pubDateStr='2026-02-25', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1790170968446, creator='13701087609', updateTime=1790219084169, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1309837032671772868, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309635220643607372, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1309837032671772869, tenantId=1146029695717560320, journalId=1227999776411738115, issueId=1309635220643607372, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=93, endPage=98, ext={EN=ArticleExt(id=1309635221998371078, articleId=1309635221826404613, tenantId=1146029695717560320, journalId=1227999776411738115, language=EN, title=Study on the Mechanism of Apoptosis in RPMI-8226 Cells Mediated by Betulinic Acid through Blocking Autophagic Flux, columnId=null, journalTitle=Pharmacy Today, columnName=null, runingTitle=null, highlight=null, articleAbstract=
OBJECTIVE To clarify the effects of betulinic acid on autophagic flux and apoptosis in RPMI-8226 multiple myeloma cells, and to explore the underlying mechanisms.
METHODS The apoptosis rate and morphological changes were detected by TUNEL and Hoechst 33258 staining methods; the activities of Caspase-3 and Caspase-8 were measured using the Caspase activity assay kits. The expression of various indicator proteins in cells was detected by Western blotting.
RESULTS Betulinic acid induced apoptosis and morphological changes in RPMI-8226 cells. Z-VAD-FMK inhibited the pro-apoptotic effect of betulinic acid, while Z-DEVD-FMK further enhanced the pro-apoptotic effect of betulinic acid. Additionally, betulinic acid increased the accumulation of autophagy-related proteins LC3B and P62, promote the activation and protein expression of Caspase-8, and subsequently increase the release of AIF. Z-VAD-FMK antagonized the effects of betulinic acid on LC3B, P62, Caspase-8 and AIF, whereas Z-DEVD-FMK synergized with betulinic acid to enhance its effects on LC3B, P62, Caspase-8 and AIF.
CONCLUSION Betulinic acid can directly activate Caspase-3 in RPMI-8226 cells. After acting on RPMI-8226 cells, it can also activate Caspase-8 by blocking autophagic flux, increase mitochondrial membrane permeability, and thereby enhance the release of AIF, thereby mediating an apoptotic process independent of Caspase-3 activation.
, authors=Ting HE, Mu PANG, Hao YANG, Dong LIN, Yinze LEI, Jun CHEN
*, authorsList=Ting HE, Mu PANG, Hao YANG, Dong LIN, Yinze LEI, Jun CHEN, authorCompany=null, correspAuthors=Jun CHEN, 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=1309635222329721095, articleId=1309635221826404613, tenantId=1146029695717560320, journalId=1227999776411738115, language=CN, title=白桦脂酸通过阻断自噬通量介导RPMI-8226细胞凋亡的机制研究, columnId=1228268589086606089, journalTitle=今日药学, columnName=论著, runingTitle=null, highlight=null, articleAbstract=
目的 明确白桦脂酸对多发性骨髓瘤RPMI-8226细胞自噬通量及凋亡的影响，并探讨其作用机制。
方法 运用Tunel及Hoechst 33258染色法检测细胞凋亡比率及细胞形态学变化；Caspase活性检测试剂盒检测Caspase-3和Caspase-8活性；Western-blot法检测细胞各指标蛋白的表达。
结果 白桦脂酸可诱导RPMI-8226细胞凋亡及形态变化，Z-VAD-FMK可抑制白桦脂酸的促凋亡作用，而Z-DEVD-FMK则可进一步增加白桦脂酸的促凋亡作用。另外，白桦脂酸可增加自噬相关蛋白LC3B和P62的积聚，促进Caspase-8活化及蛋白表达增加，进而增加AIF的释放；Z-VAD-FMK可拮抗白桦脂酸对LC3B、P62、Caspase-8及AIF的作用；反之，Z-DEVD-FMK可协同白桦脂酸对LC3B、P62、Caspase-8及AIF的作用。
结论 白桦脂酸作用于RPMI-8226细胞后，除能直接激活Caspase-3之外，还可通过阻断细胞自噬通量后激活Caspase-8，增加线粒体膜通透性，使AIF释放增加，从而介导以不依赖Caspase-3活化的凋亡过程。
, authors=何婷, 庞牧, 杨昊, 林栋, 雷吟泽, 陈军
*, authorsList=何婷, 庞牧, 杨昊, 林栋, 雷吟泽, 陈军, authorCompany=null, correspAuthors=陈军, authorNote=
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