Article(id=1322923582686376558, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2025.05.021, 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=1793339160843, onlineDateStr=2026-10-30, pubDate=1746806400000, pubDateStr=2025-05-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793339160843, onlineIssueDateStr=2026-10-30, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793339160843, creator=13701087609, updateTime=1793339160843, updator=13701087609, issue=Issue{id=1322923490592043032, tenantId=1146029695717560320, journalId=1255847919539208197, year='2025', volume='43', issue='5', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1746806400000', pubDateStr='2025-05-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1793339138887, creator='13701087609', updateTime=1793340572227, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322929502539612595, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322929502539612596, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1322923490592043032, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=99, endPage=104, ext={EN=ArticleExt(id=1322923582896091759, articleId=1322923582686376558, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Research Progress of Active Ingredients of Chinese Medicines Regulating Mitochondrial Apoptosis in Anti-Tumor, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=

The prevention and treatment of malignant tumors has always been a hot topic for oncologists around the world. Mitochondrion is a key organelle that can regulate the internal metabolism of tumor cells and always affect the occurrence and development of tumors. Apoptosis is an important regulatory mechanism for cells to maintain their internal environment. Mitochondrial apoptosis pathway is one of the main pathways to promote apoptosis，and the induction of mitochondrial apoptosis in tumor cells is an important target for anti-tumor. Studies have shown that the active ingredients of many Chinese medicines，such as flavonoids，lactones，alkaloids，terpenoids，glycosides and quinones，can increase the expressions of pro-apoptotic proteins such as Bax，Bad and Bim，and decrease the expressions of anti-apoptotic proteins such as Bcl-2 and Bcl-xL，down-regulate the mitochondrial membrane potential level，increase the permeability of mitochondrial membrane，release a large number of apoptotic factors，activate the Caspase cascade reaction，and finally induce the endogenous apoptotic pathway of tumor cells，and inhibit the proliferation and invasion of tumor cells by regulating PI3K/AKT，TLR9/MyD88，p38 MAPK，ERK1/2，Notch/JAK/STAT and other signaling pathways. This article summarized the research results of the specific mechanism of the active ingredients of Chinese medicines regulating the mitochondrial apoptosis pathway in recent years，and discussed the aspects of the active ingredients of Chinese medicines regulating the mitochondrial apoptosis pathway to enhance the anti-tumor effect，in order to provide new research ideas for the anti-tumor treatment of traditional Chinese medicine and further improve the effectiveness of clinical anti-tumor treatment.

, authors=Chengzhi WANG¹, Yifan LIU¹, Xiaoqing ZHANG², Gelei ZHAO¹, Shan ZHANG¹, Peimin LIU¹, Dongdong LI¹, authorsList=Chengzhi WANG, Yifan LIU, Xiaoqing ZHANG, Gelei ZHAO, Shan ZHANG, Peimin LIU, Dongdong LI, authorCompany=null, correspAuthors=Peimin LIU, Dongdong LI, 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=1322923583667843698, articleId=1322923582686376558, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=中药活性成分调控线粒体凋亡在抗肿瘤中的研究进展, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=

恶性肿瘤的防治工作一直是全球肿瘤学者共同关注的热门话题。线粒体是一种可以调节肿瘤细胞内部代谢的关键细胞器，始终影响着肿瘤的发生发展。细胞凋亡是细胞维持自身内环境的重要调节机制，线粒体凋亡途径是促进细胞凋亡的主要途径之一，而诱导肿瘤细胞线粒体凋亡途径是抗肿瘤的重要靶点。研究发现，多种中药活性成分如黄酮类、内酯类、生物碱类、萜类、苷类以及醌类等可以通过调控磷脂酰肌醇3-激酶（Phosphatidylin-ositol-3-kinase，PI3K）/蛋白激酶B（Protein kinase B，AKT/PKB）、Toll样受体9（Toll-like receptors，TLR9）/髓样分化因子88（Myeloid differentiation primary response 88，MyD88）、p38丝裂原活化蛋白激酶（p38 mitogen-activated protein kinase，p38 MAPK）、细胞外信号调节激酶1/2（Extracellular-regulated kinase 1/2，ERK1/2）以及Notch/Janus激酶（Janus kinases，JAK）/信号转导子与转录激活因子（Signal transducers and activators of transcription，STAT）等信号通路，提高B淋巴细胞瘤-2基因相关的x基因（B cell lymphoma-2 associated X，Bax）、Bcl-2基因相关启动子（Bcl-2 associated death promoter，Bad）等促凋亡蛋白的表达，降低B淋巴细胞瘤-2基因（B cell lymphoma-2，Bcl-2）、B淋巴细胞瘤-xL（B cell lymphoma-xl，Bcl-xL）等抑凋亡蛋白的表达，下调线粒体膜电位水平，增加线粒体膜通透性，释放大量凋亡因子，激活半胱氨酸天冬氨酸蛋白酶（Cystein asparate protease，Caspase）级联反应，最终诱导肿瘤细胞内源性凋亡途径，抑制肿瘤细胞的增殖和侵袭。通过总结近年来中药活性成分调控线粒体凋亡途径具体作用机制的研究成果，从中药活性成分调控线粒体凋亡途径以增强抗肿瘤作用方面进行论述，以期为中医药抗肿瘤治疗提供新的研究思路，进一步提高临床抗肿瘤治疗的有效性。

, authors=王成志¹, 刘一帆¹, 张晓青², 赵戈蕾¹, 张山¹, 刘培民¹, 李东东¹, authorsList=王成志, 刘一帆, 张晓青, 赵戈蕾, 张山, 刘培民, 李东东, authorCompany=null, correspAuthors=刘培民, 李东东, authorNote=, correspAuthorsNote=, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=bEYQp8JLcri1zLUaVCBDIg==, magXml=gNcRaEA9WqO1SEfa1GZ8Dg==, pdfUrl=null, pdf=ypq6vgVyq1mmSF0b/TOUgQ==, pdfFileSize=2352548, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=N+8L8k5Ly1uOXoT7D5yJ8A==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=bo7It8GHxabw2W451vZOMw==, mapNumber=null, fund=null)}, authors=[Author(id=1322923585777578618, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, orderNo=0, firstName=null, middleName=null, lastName=null, nameCn=null, orcid=null, stid=null, country=null, authorPic=null, dead=0, email=null, emailSecond=null, emailThird=null, correspondingAuthor=0, authorType=1, ext={EN=AuthorExt(id=1322923585882436220, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, authorId=1322923585777578618, language=EN, stringName=Chengzhi WANG, firstName=Chengzhi, middleName=null, lastName=WANG, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=¹, address=^1.The Second Affiliated Hospital of Henan University of Chinese Medicine，Zhengzhou 450002，Henan，China, bio=null, bioImg=null, bioContent=null, aboutCorrespAuthor=null), CN=AuthorExt(id=1322923586016653949, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, authorId=1322923585777578618, language=CN, stringName=王成志, firstName=null, middleName=null, lastName=null, prefix=null, suffix=null, authorComment=null, nameInitials=null, affiliation=null, department=null, xref=¹, address=^1.河南中医药大学第二附属医院，河南 郑州 450002, bio={"content":"

王成志（1998-），男，河南驻马店人，硕士在读，研究方向：中医药防治恶性肿瘤的临床及基础。

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王成志（1998-），男，河南驻马店人，硕士在读，研究方向：中医药防治恶性肿瘤的临床及基础。

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unstructuredReference=王海波，罗园园，冯心怡，等. 南蛇藤提取物通过破坏线粒体结构促进胃癌AGS细胞凋亡的机制［J］. 中国实验方剂学杂志，2022，28（18）：46-53., articleTitle=南蛇藤提取物通过破坏线粒体结构促进胃癌AGS细胞凋亡的机制, refAbstract=null), Reference(id=1322923596791821031, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, doi=null, pmid=null, pmcid=null, year=2022, volume=26, issue=30, pageStart=4873, pageEnd=4878, url=null, language=null, rfNumber=［59］, rfOrder=58, authorNames=吴慧婷, 朱大诚, 徐笑明, journalName=中国组织工程研究, refType=null, unstructuredReference=吴慧婷，朱大诚，徐笑明，等. 川楝子醇提物通过线粒体途径诱导白血病CEM细胞的凋亡［J］. 中国组织工程研究，2022，26（30）：4873-4878., articleTitle=川楝子醇提物通过线粒体途径诱导白血病CEM细胞的凋亡, refAbstract=null)], funds=[Fund(id=1322923590605222568, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, awardId=82204981, language=CN, fundingSource=国家自然科学基金项目(82204981), fundOrder=null, country=null), Fund(id=1322923590672331433, tenantId=1146029695717560320, journalId=1255847919539208197, 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分类	中药活性成分	来源	调控线粒体凋亡具体作用机制	作用肿瘤	参考文献
黄酮类	丹参酮ⅡA	丹参	降低ATP含量和耗氧量，下调线粒体膜电位，提高Cyt C、TSPO、Caspase-3、Caspase-9表达	肝癌	［13］
	姜黄素	姜黄	抑制Notch1信号通路，提高Bax、Caspase-3、Caspase-9表达，降低Bcl-2表达	白血病	［14］
	姜黄素衍生物C086	姜黄	抑制PI3K-AKT通路，降低Bcl-2表达，提高Caspase-3、Bax、Cyt C表达	肝癌	［15］
	丹皮酚	牡丹皮	提高Bax、Cyt C、cleaved Caspase-9表达，降低Bcl-2表达	卵巢癌	［16］
内酯类	青蒿琥酯	青蒿	提高Bax表达，降低Bcl-2、Bcl-xL表达	结直肠癌	［17］
			提高Bax、Caspase-3表达，下调Bcl-2表达	胃癌	［18］
	穿心莲内酯脂质体	穿心莲	促进ROS产生，提高Caspase-3活性，破坏线粒体膜电位，降低BCl-2表达，提高Bax表达	胃癌	［19］
	鸦胆子苦醇	鸦胆子	激活TLR9-MyD88信号通路，提高Bax表达，降低线粒体膜电位，促进Cyt C释放	宫颈癌	［20］
	木香烃内酯	木香	提高Bax、Caspases-3、8、9表达，降低Bcl-2表达	肝癌	［21］
			提高Bax、cleaved Caspase-3/7/9、表达，降低Bcl-2、pro-Caspase-3/7/9表达	胃癌	［22］
			提高p53、Bax表达，降低Bcl-2表达，激活Caspase-3级联反应	肺癌	［23］
			释放更多ROS，降低线粒体跨膜电位，改善Bcl-2/Bax比例	骨肉瘤	［24］
生物碱类	苦参碱	苦参	调控Mst1-JNK信号通路，降低线粒体膜电位，提高Bax、Bad、Caspase-9表达	肝癌	［25］
			降低ATP含量和线粒体膜电位水平，提高Cyt C、Bax、Caspase-9表达，降低Bcl-2表达	结直肠癌	［26］
			降低Bcl-2表达，提高Bax和cleaved Caspase-3表达	大肠癌	［27］
			抑制PINK1/Parkin信号通路活化，降低细胞线粒体膜电位，提高Bax表达，降低Bcl-2表达	骨肉瘤	［28］
	防己诺林碱	防己	降低Bcl-2蛋表达，提高Bax、Caspase-3表达	前列腺癌	［29］
	贝母素乙	贝母	阻断PI3K/AKT信号通路，提高Cyt C、Bax、cleaved-Caspase-3表达，降低Bcl-2表达	乳腺癌	［30］
	盐酸青藤碱	青风藤	诱导Cyt C释放，导致线粒体膜电位损坏	胃癌	［31］
	马钱子碱	马钱子	下调线粒体膜电位，改变线粒体结构，增加线粒体膜通透性，促进Cyt C释放	结直肠癌	［32］
	小檗碱	黄连	抑制NF-κB信号通路，破坏线粒体功能，提高Caspase-3、Bax表达，降低Bcl-2表达	淋巴瘤	［33］
萜类	雷公藤甲素	雷公藤	提高ROS、Bax、Caspase-3的表达，降低BCl-2表达	肝癌	［34］
	冬凌草甲素	冬凌草	提高Cyt C、Bax表达，降低Bcl-2表达，提高Caspase-3、Caspase-9活性	宫颈癌	［35］
	雷酚萜	南蛇藤	降低Bcl-2、Bcl-xL表达，提高Bax表达	胃癌	［36］
	熊果酸	夏枯草	抑制CXCR12/CXCR4/CXCR7信号轴，提高Bax的表达，降低Bcl-2表达	甲状腺癌	［37］
	过氧麦角甾醇	灵芝	促进ROS产生，提高Bax、Cyt C、Caspase-3/9表达，降低Bcl-2表达	肝癌	［38］
	山楂酸	山楂	提高Bax、Caspase-3表达，降低Bcl-2表达	宫颈癌	［39］
	土荆皮乙酸	土荆皮	提高Bax、Caspase-3和Caspase-9表达，降低Bcl-2表达	食管癌	［40］
			提高Bax/Bcl-2比例，加快Caspase-3、PARP分裂	肝癌	［41］
	蒲公英萜醇	蒲公英	通过抑制PI3K/AKT信号通路，提高Bax、Cyt C表达，降低Bcl-2表达	宫颈癌、胃癌	［42］
	莪术醇	莪术	激活p38 MAPK信号通路，提高Cyt C、Bax、Cleaved-Caspase-3表达，降低Bcl-2表达	舌癌	［43］
	甘草酸	甘草	降低线粒体膜电位，提高Caspase-3/8/9活性	宫颈癌	［44］
多糖类	白术多糖	白术	降低Bcl-2表达，提高Cyt C、Bax、cleaved-Caspase3表达	子宫内膜癌	［45］
	黄芪多糖	黄芪	降低线粒体膜电位，诱导Cyt C产生，提高Bax/Bcl-2比例，增加Caspase-9、Caspase-3表达	胃癌	［46］
	红芪多糖	红芪	降低线粒体膜电位水平，提高Bax、cleaved PARP、cleaved Caspase-3、cleaved Caspase-9表达	皮肤癌	［47］
	灵芝多糖	灵芝	降低Bcl-2表达，提高Caspase-3表达	胃癌	［48］
苷类	重楼皂苷Ⅶ	重楼	激活PP2A/AKT信号通路，促进ROS产生，提高Cyt C、Bax表达，降低Bcl-2表达	卵巢癌	［49］
	重楼皂苷A		促进ROS产生，降低线粒体膜电位，下调pro-Caspase-9、pro-Caspase-3的表达，激活Caspase-9级联反应	胃癌	［50］
	重楼皂苷Ⅱ		提高Bax/Bcl-2比例，降低线粒体膜电位，提高cleaved Caspase 3和cleaved PARP表达	骨肉瘤	［51］
	人参皂苷CK	人参	通过调控ERK1/2信号通路，降低线粒体膜电位，提高Bax、Cyt C和Cleaved Caspase-3表达，降低Bcl-2表达	肝癌	［52］
醌类	大黄素	大黄	增加ROS产生、提高Ca2+表达，降低ATP含量，增加Caspase-3活性	肝癌	［53］
	大黄酸		抑制NOTCH/JAK/STAT信号通路，降低膜电位水平，提高Bax、Caspase-3表达，降低BCL-2表达	胃癌	［54］
其他	南方红豆杉水提物	南方红豆杉	提高ROS、LDH和MDA含量，降低SOD活性，降线粒体膜电位以及Bcl-2表达，促进Caspase-3和Caspase-9活化	口腔癌	［55］
	紫檀芪	檀香	促进ROS产生，降低线粒体膜电位，提高Apaf-1、AIF、Bax、Cyt C、cleaved Caspase-3/9表达，降低Bcl-2表达	结直肠癌	［56］
	蒲公英根提取物	蒲公英	破坏细胞线粒体膜电位，激活Caspase-3/9，降低Bcl-2表达	乳腺癌	［57］
	南蛇藤提取物	南蛇藤	提高SOD1表达，降低VDAC、PHB1、HSP60表达，破坏线粒体结构，损伤线粒体包膜，加速Cyt C释放	胃癌	［58］
	川楝子醇提物	川楝子	提高Bax、Cyt C、Caspase-9和Caspase-3表达，降低Bcl-2表达	白血病	［59］

), ArticleFig(id=1322923590496170663, tenantId=1146029695717560320, journalId=1255847919539208197, articleId=1322923582686376558, language=CN, label=表1, caption=

中药活性成分调控线粒体凋亡抗肿瘤作用机制总结

, figureFileSmall=null, figureFileBig=null, tableContent=

分类	中药活性成分	来源	调控线粒体凋亡具体作用机制	作用肿瘤	参考文献
黄酮类	丹参酮ⅡA	丹参	降低ATP含量和耗氧量，下调线粒体膜电位，提高Cyt C、TSPO、Caspase-3、Caspase-9表达	肝癌	［13］
	姜黄素	姜黄	抑制Notch1信号通路，提高Bax、Caspase-3、Caspase-9表达，降低Bcl-2表达	白血病	［14］
	姜黄素衍生物C086	姜黄	抑制PI3K-AKT通路，降低Bcl-2表达，提高Caspase-3、Bax、Cyt C表达	肝癌	［15］
	丹皮酚	牡丹皮	提高Bax、Cyt C、cleaved Caspase-9表达，降低Bcl-2表达	卵巢癌	［16］
内酯类	青蒿琥酯	青蒿	提高Bax表达，降低Bcl-2、Bcl-xL表达	结直肠癌	［17］
			提高Bax、Caspase-3表达，下调Bcl-2表达	胃癌	［18］
	穿心莲内酯脂质体	穿心莲	促进ROS产生，提高Caspase-3活性，破坏线粒体膜电位，降低BCl-2表达，提高Bax表达	胃癌	［19］
	鸦胆子苦醇	鸦胆子	激活TLR9-MyD88信号通路，提高Bax表达，降低线粒体膜电位，促进Cyt C释放	宫颈癌	［20］
	木香烃内酯	木香	提高Bax、Caspases-3、8、9表达，降低Bcl-2表达	肝癌	［21］
			提高Bax、cleaved Caspase-3/7/9、表达，降低Bcl-2、pro-Caspase-3/7/9表达	胃癌	［22］
			提高p53、Bax表达，降低Bcl-2表达，激活Caspase-3级联反应	肺癌	［23］
			释放更多ROS，降低线粒体跨膜电位，改善Bcl-2/Bax比例	骨肉瘤	［24］
生物碱类	苦参碱	苦参	调控Mst1-JNK信号通路，降低线粒体膜电位，提高Bax、Bad、Caspase-9表达	肝癌	［25］
			降低ATP含量和线粒体膜电位水平，提高Cyt C、Bax、Caspase-9表达，降低Bcl-2表达	结直肠癌	［26］
			降低Bcl-2表达，提高Bax和cleaved Caspase-3表达	大肠癌	［27］
			抑制PINK1/Parkin信号通路活化，降低细胞线粒体膜电位，提高Bax表达，降低Bcl-2表达	骨肉瘤	［28］
	防己诺林碱	防己	降低Bcl-2蛋表达，提高Bax、Caspase-3表达	前列腺癌	［29］
	贝母素乙	贝母	阻断PI3K/AKT信号通路，提高Cyt C、Bax、cleaved-Caspase-3表达，降低Bcl-2表达	乳腺癌	［30］
	盐酸青藤碱	青风藤	诱导Cyt C释放，导致线粒体膜电位损坏	胃癌	［31］
	马钱子碱	马钱子	下调线粒体膜电位，改变线粒体结构，增加线粒体膜通透性，促进Cyt C释放	结直肠癌	［32］
	小檗碱	黄连	抑制NF-κB信号通路，破坏线粒体功能，提高Caspase-3、Bax表达，降低Bcl-2表达	淋巴瘤	［33］
萜类	雷公藤甲素	雷公藤	提高ROS、Bax、Caspase-3的表达，降低BCl-2表达	肝癌	［34］
	冬凌草甲素	冬凌草	提高Cyt C、Bax表达，降低Bcl-2表达，提高Caspase-3、Caspase-9活性	宫颈癌	［35］
	雷酚萜	南蛇藤	降低Bcl-2、Bcl-xL表达，提高Bax表达	胃癌	［36］
	熊果酸	夏枯草	抑制CXCR12/CXCR4/CXCR7信号轴，提高Bax的表达，降低Bcl-2表达	甲状腺癌	［37］
	过氧麦角甾醇	灵芝	促进ROS产生，提高Bax、Cyt C、Caspase-3/9表达，降低Bcl-2表达	肝癌	［38］
	山楂酸	山楂	提高Bax、Caspase-3表达，降低Bcl-2表达	宫颈癌	［39］
	土荆皮乙酸	土荆皮	提高Bax、Caspase-3和Caspase-9表达，降低Bcl-2表达	食管癌	［40］
			提高Bax/Bcl-2比例，加快Caspase-3、PARP分裂	肝癌	［41］
	蒲公英萜醇	蒲公英	通过抑制PI3K/AKT信号通路，提高Bax、Cyt C表达，降低Bcl-2表达	宫颈癌、胃癌	［42］
	莪术醇	莪术	激活p38 MAPK信号通路，提高Cyt C、Bax、Cleaved-Caspase-3表达，降低Bcl-2表达	舌癌	［43］
	甘草酸	甘草	降低线粒体膜电位，提高Caspase-3/8/9活性	宫颈癌	［44］
多糖类	白术多糖	白术	降低Bcl-2表达，提高Cyt C、Bax、cleaved-Caspase3表达	子宫内膜癌	［45］
	黄芪多糖	黄芪	降低线粒体膜电位，诱导Cyt C产生，提高Bax/Bcl-2比例，增加Caspase-9、Caspase-3表达	胃癌	［46］
	红芪多糖	红芪	降低线粒体膜电位水平，提高Bax、cleaved PARP、cleaved Caspase-3、cleaved Caspase-9表达	皮肤癌	［47］
	灵芝多糖	灵芝	降低Bcl-2表达，提高Caspase-3表达	胃癌	［48］
苷类	重楼皂苷Ⅶ	重楼	激活PP2A/AKT信号通路，促进ROS产生，提高Cyt C、Bax表达，降低Bcl-2表达	卵巢癌	［49］
	重楼皂苷A		促进ROS产生，降低线粒体膜电位，下调pro-Caspase-9、pro-Caspase-3的表达，激活Caspase-9级联反应	胃癌	［50］
	重楼皂苷Ⅱ		提高Bax/Bcl-2比例，降低线粒体膜电位，提高cleaved Caspase 3和cleaved PARP表达	骨肉瘤	［51］
	人参皂苷CK	人参	通过调控ERK1/2信号通路，降低线粒体膜电位，提高Bax、Cyt C和Cleaved Caspase-3表达，降低Bcl-2表达	肝癌	［52］
醌类	大黄素	大黄	增加ROS产生、提高Ca2+表达，降低ATP含量，增加Caspase-3活性	肝癌	［53］
	大黄酸		抑制NOTCH/JAK/STAT信号通路，降低膜电位水平，提高Bax、Caspase-3表达，降低BCL-2表达	胃癌	［54］
其他	南方红豆杉水提物	南方红豆杉	提高ROS、LDH和MDA含量，降低SOD活性，降线粒体膜电位以及Bcl-2表达，促进Caspase-3和Caspase-9活化	口腔癌	［55］
	紫檀芪	檀香	促进ROS产生，降低线粒体膜电位，提高Apaf-1、AIF、Bax、Cyt C、cleaved Caspase-3/9表达，降低Bcl-2表达	结直肠癌	［56］
	蒲公英根提取物	蒲公英	破坏细胞线粒体膜电位，激活Caspase-3/9，降低Bcl-2表达	乳腺癌	［57］
	南蛇藤提取物	南蛇藤	提高SOD1表达，降低VDAC、PHB1、HSP60表达，破坏线粒体结构，损伤线粒体包膜，加速Cyt C释放	胃癌	［58］
	川楝子醇提物	川楝子	提高Bax、Cyt C、Caspase-9和Caspase-3表达，降低Bcl-2表达	白血病	［59］

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