Article(id=1240730052392972857, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202501139, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1736265600000, receivedDateStr=2025-01-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1773742696140, onlineDateStr=2026-03-17, pubDate=1745510400000, pubDateStr=2025-04-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773742696140, onlineIssueDateStr=2026-03-17, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773742696140, creator=13701087609, updateTime=1773742696140, updator=13701087609, issue=Issue{id=1240730050669113883, tenantId=1146029695717560320, journalId=1227665162245664772, year='2025', volume='52', issue='8', pageStart='1345', pageEnd='1536', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773742695728, creator=13701087609, updateTime=1773742807836, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1240730520988995837, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1240730520988995838, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1240730050669113883, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1517, endPage=1524, ext={EN=ArticleExt(id=1240730052678185544, articleId=1240730052392972857, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=Mechanistic study of curcumin in the tertiary prevention strategy of non-small cell lung cancer, columnId=1228016569138213037, journalTitle=Modern Preventive Medicine, columnName=Clinical Medicine and Prevention, runingTitle=null, highlight=null, articleAbstract=
Non-small cell lung cancer is a common malignant tumor with soaring incidence and mortality rates. Although various existing treatment methods have extended the survival period of patients, the prognosis remains poor. Therefore, standardizing the Tertiary prevention strategy for lung cancer is extremely crucial. The Tertiary prevention strategy for lung cancer is divided into: primary cause prevention, secondary early prevention, and tertiary clinical prevention. Curcumin has become a hotspot in lung cancer prevention due to its broad biological activity and low toxicity. Derived from turmeric, it possesses various pharmacological activities, capable of inhibiting lung cancer cell proliferation, inducing apoptosis, and resisting invasion and metastasis, showing significant anti-tumor potential, and has application potential in the Tertiary prevention of lung cancer. This article reviews the latest achievements of curcumin and its combination with chemotherapy drugs from January 2010 to January 2025 in databases such as PubMed and CNKI, elucidating its multifaceted roles in the Tertiary prevention strategy of lung cancer. However, curcumin faces issues such as rapid metabolism, poor oral bioavailability, and limited water solubility, slightly hindering its clinical application, but it still holds promise as a potential medication or auxiliary means for theTertiary prevention of non-small cell lung cancer.
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非小细胞肺癌是常见恶性肿瘤,发病率与死亡率飙升,虽现有多种治疗手段延长了患者生存期,但其预后仍不佳,因此规范肺癌三级预防策略极为关键。肺癌三级预防策略分为:一级病因预防,二级三早预防,三级临床预防。姜黄素因生物活性广、毒性低,成肺癌预防热点。它源于姜黄,有多种药理活性,能抑制肺癌细胞增殖、诱导凋亡、抗侵袭转移,抗肿瘤潜能显著,在肺癌三级预防中有应用潜力。本文梳理PubMed、中国知网等数据库2010年1月—2025年1月中姜黄素及其联合化疗药物的最新成果,阐述在肺癌三级预防策略中多方面作用。不过,姜黄素存在代谢快、口服生物利用度差、水溶性有限等问题,稍微阻碍其临床应用,但它仍有望成为非小细胞肺癌三级预防潜在用药或辅助手段。
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本刊刊出的所有文章不代表中华预防医学会和本刊编委会的观点,除非特别声明。, copyrightOwner=中华预防医学会和四川大学华西公共卫生学院, extLink=null, articleAbsUrl=null, sourceXml=Ddtfe1s/gQw1JBFoKx2oSA==, magXml=wdTL/AnyIYmDlK7cWnVZdQ==, pdfUrl=null, pdf=hs7BG3rbT3HDRIuIDZCMaQ==, pdfFileSize=1231841, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=b7LnBpNY35rCEApnW0jHzg==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=YE5fr/Io6Z92sbMyjdOo3g==, mapNumber=null, authorCompany=null, fund=null, authors=
李罗杰(1999—),男,硕士在读,研究方向:肿瘤康复的中医养生基础和临床研究
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1.成都中医药大学养生康复学院,四川 成都 610000)]), AuthorCompany(id=1241070734462743026, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, xref=2., ext=[AuthorCompanyExt(id=1241070734475325942, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, companyId=1241070734462743026, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=
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Curcumin controls the levels of proliferation, metastasis, and invasion in non-small cell lung cancer cells. By regulating the expression of key signaling pathways in cells, curcumin inhibits the survival of lung cancer cells, thereby suppressing tumor cell proliferation, invasion, and metastasis, figureFileSmall=wcA7RGOBljBl/xH+swFwbw==, figureFileBig=PQOSV8k3pnGddorfiw/aVQ==, tableContent=null), ArticleFig(id=1241070739734983487, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=CN, label=图1, caption=
姜黄素控制抗非小细胞肺癌细胞的增殖、转移和侵袭水平。姜黄素通过调节细胞中关键信号通路的表达,抑制肺癌细胞的存活,从而抑制肿瘤细胞的增殖、侵袭和转移, figureFileSmall=wcA7RGOBljBl/xH+swFwbw==, figureFileBig=PQOSV8k3pnGddorfiw/aVQ==, tableContent=null), ArticleFig(id=1241070739865006919, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=EN, label=Fig.2, caption=
Curcumin modulates the epigenetic level in non-small cell lung cancer. Numerous miRNAs are abnormally expressed in tumor cells. Curcumin regulates different pathways and the transcriptional regulation of various tumor-related lncRNAs by manipulating certain key miRNAs, thereby achieving the goal of preventing and treating non-small cell lung cancer, figureFileSmall=fMizNCsVUzymHwBUxk+z/A==, figureFileBig=b5OmBdDu7613BnrvopixEA==, tableContent=null), ArticleFig(id=1241070739944698698, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=CN, label=图2, caption=
姜黄素控制抗非小细胞肺癌表观遗传学水平。大量miRNA在肿瘤细胞中异常表达,姜黄素通过操纵某些关键miRNA来调控不同的通路以及多种肿瘤相关lncRNA的转录调控,从而达到防治非小细胞肺癌的目的, figureFileSmall=fMizNCsVUzymHwBUxk+z/A==, figureFileBig=b5OmBdDu7613BnrvopixEA==, tableContent=null), ArticleFig(id=1241070740028584784, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=EN, label=Table 1, caption=
Effects of curcumin on autophagy and apoptosis of non-small cell lung cancer cells
, figureFileSmall=null, figureFileBig=null, tableContent=
| 细胞类型 | 作用机理 | 结果 | 参考文献 |
|---|
| A549 | AMPK↑ | 抑制细胞生长克服细胞对EGFR-TKIs耐药性 | [29] |
| A549 | miR-192-5p↑PI3K/Akt↓ | 抑制细胞增殖诱导细胞凋亡 | [30] |
| A549 | ROS↓SOD、CAT↑Akt/GSK3β↑ | 通过溶酶体预防线粒体功能障碍抑制细胞凋亡 | [31][32] |
| A549 | 14-3-3↓Bad↑ | 促进向线粒体转位诱导细胞凋亡 | [33] |
| A549 | PI3K/AKT/mTOR↓PI3K/AKT/PKC↓ | 促进细胞凋亡和自噬 | [34][35] |
| A549 | Bcl-2、Bcl-xl↓Bax↑ | 促进线粒体膜电位的丧失加速细胞凋亡 | [36] |
| A549/H1299 | ACSL4↑SLC7A11、GPX4↓ | 诱导细胞发生铁死亡抑制细胞生长促进细胞死亡 | [37] |
| A549/H1299 | EGFR、PI3K、P-AKT/AKT↓Caspase-3、PARP↑ | 抑制细胞异常增殖和迁移诱导细胞凋亡 | [38] |
), ArticleFig(id=1241070740154413909, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=CN, label=表1, caption=
姜黄素对非小细胞肺癌细胞自噬和凋亡的影响
, figureFileSmall=null, figureFileBig=null, tableContent=
| 细胞类型 | 作用机理 | 结果 | 参考文献 |
|---|
| A549 | AMPK↑ | 抑制细胞生长克服细胞对EGFR-TKIs耐药性 | [29] |
| A549 | miR-192-5p↑PI3K/Akt↓ | 抑制细胞增殖诱导细胞凋亡 | [30] |
| A549 | ROS↓SOD、CAT↑Akt/GSK3β↑ | 通过溶酶体预防线粒体功能障碍抑制细胞凋亡 | [31][32] |
| A549 | 14-3-3↓Bad↑ | 促进向线粒体转位诱导细胞凋亡 | [33] |
| A549 | PI3K/AKT/mTOR↓PI3K/AKT/PKC↓ | 促进细胞凋亡和自噬 | [34][35] |
| A549 | Bcl-2、Bcl-xl↓Bax↑ | 促进线粒体膜电位的丧失加速细胞凋亡 | [36] |
| A549/H1299 | ACSL4↑SLC7A11、GPX4↓ | 诱导细胞发生铁死亡抑制细胞生长促进细胞死亡 | [37] |
| A549/H1299 | EGFR、PI3K、P-AKT/AKT↓Caspase-3、PARP↑ | 抑制细胞异常增殖和迁移诱导细胞凋亡 | [38] |
), ArticleFig(id=1241070740246688603, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=EN, label=Table 2, caption=
Binding of curcumin and some small molecule compounds tonon-small cell lung cancer
, figureFileSmall=null, figureFileBig=null, tableContent=
| 姜黄素+无机化疗药物 |
|---|
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
|---|
| 姜黄素+顺铂 | A549 | P-gp↓AKT/ERK↓ | 促进细胞凋亡抑制迁移和侵袭提高细胞对顺铂的敏感性 | [63] |
| 姜黄素+卡铂 | A549 | AKT-IKKα轴↓NF-κB、ERK1/2↓ | 促进细胞凋亡 | [64] |
| 姜黄素+有机化疗药物 |
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
| 姜黄素+紫杉醇 | A549 | miR-30c-5p↑MTA1↓ | 增加紫杉醇耐药细胞的紫杉醇敏感性 | [65] |
| 姜黄素+吉西他滨 | A549/GEM | lncRNA MEG3↑p53↑ | 提高细胞系多重耐药敏感性减少细胞迁移和入侵 | [66] |
| 姜黄素+甲氨蝶呤 | A549 | P-gp↓ | 降低Calu-3细胞活力 | [67] |
| 姜黄素+靶向药物 |
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
| 姜黄素+吉非替尼 | H157/H1299 | Sp1、EGFR↓ERK/MEK↓ | 阻断Sp1和HADC1相互作用克服对吉非替尼的耐药性增强EGFR-TKI的疗效 | [68] |
| 姜黄素+克唑替尼 | A549 | miR-142-5p↑ | 增加克唑替尼的细胞毒性诱导肿瘤细胞凋亡 | [69] |
| 姜黄素+厄洛替尼 | A549 | EGFR↓ | 增加厄洛替尼耐药细胞敏感性介导厄洛替尼耐药细胞凋亡 | [70] |
), ArticleFig(id=1241070740372517732, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1240730052392972857, language=CN, label=表2, caption=
姜黄素和一些小分子化合物对非小细胞肺癌的结合
, figureFileSmall=null, figureFileBig=null, tableContent=
| 姜黄素+无机化疗药物 |
|---|
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
|---|
| 姜黄素+顺铂 | A549 | P-gp↓AKT/ERK↓ | 促进细胞凋亡抑制迁移和侵袭提高细胞对顺铂的敏感性 | [63] |
| 姜黄素+卡铂 | A549 | AKT-IKKα轴↓NF-κB、ERK1/2↓ | 促进细胞凋亡 | [64] |
| 姜黄素+有机化疗药物 |
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
| 姜黄素+紫杉醇 | A549 | miR-30c-5p↑MTA1↓ | 增加紫杉醇耐药细胞的紫杉醇敏感性 | [65] |
| 姜黄素+吉西他滨 | A549/GEM | lncRNA MEG3↑p53↑ | 提高细胞系多重耐药敏感性减少细胞迁移和入侵 | [66] |
| 姜黄素+甲氨蝶呤 | A549 | P-gp↓ | 降低Calu-3细胞活力 | [67] |
| 姜黄素+靶向药物 |
| 项目 | 细胞类型 | 机制 | 结果 | 参考文献 |
| 姜黄素+吉非替尼 | H157/H1299 | Sp1、EGFR↓ERK/MEK↓ | 阻断Sp1和HADC1相互作用克服对吉非替尼的耐药性增强EGFR-TKI的疗效 | [68] |
| 姜黄素+克唑替尼 | A549 | miR-142-5p↑ | 增加克唑替尼的细胞毒性诱导肿瘤细胞凋亡 | [69] |
| 姜黄素+厄洛替尼 | A549 | EGFR↓ | 增加厄洛替尼耐药细胞敏感性介导厄洛替尼耐药细胞凋亡 | [70] |
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