Article(id=1308840556168573066, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1308840287129141340, articleNumber=null, orderNo=null, doi=10.16438/j.0513-4870.2025-0648, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1749398400000, receivedDateStr=2025-06-09, revisedDate=1766073600000, revisedDateStr=2025-12-19, acceptedDate=null, acceptedDateStr=null, onlineDate=1789981505671, onlineDateStr=2026-09-21, pubDate=1775923200000, pubDateStr=2026-04-12, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1789981505671, onlineIssueDateStr=2026-09-21, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1789981505671, creator=13701087609, updateTime=1789981505671, updator=13701087609, issue=Issue{id=1308840287129141340, tenantId=1146029695717560320, journalId=1189982191388893191, year='2026', volume='61', issue='4', pageStart='1001', pageEnd='1434', issueExtLink='null', onlineDate='null', pubDate='1775923200000', pubDateStr='2026-04-12', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1789981441528, creator='13701087609', updateTime=1789984228828, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1308851977992368434, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1308840287129141340, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1308851977992368435, tenantId=1146029695717560320, journalId=1189982191388893191, issueId=1308840287129141340, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1190, endPage=1198, ext={EN=ArticleExt(id=1308840557888237707, articleId=1308840556168573066, tenantId=1146029695717560320, journalId=1189982191388893191, language=EN, title=Cryptotanshinone inhibits colorectal cancer cell proliferation by inducing ferroptosis via GPX4, columnId=1190335348761793317, journalTitle=Acta Pharmaceutica Sinica, columnName=Original Articles, runingTitle=null, highlight=null, articleAbstract=

This study aims to investigate the inhibitory effects of cryptotanshinone (CPT) on colorectal cancer (CRC) both in vitro and in vivo, and to explore its potential mechanism of action based on ferroptosis. CRC HCT116 and HCT8 cells were treated with different concentrations of CPT. Cell counting, colony formation assays, and Annexin V/PI staining revealed that CPT significantly inhibited CRC cell viability and proliferation and promoted apoptosis. A CRC patient-derived organoid (PDO) (in accordance with the regulations of the Nankai University Biomedical Ethics Committee approval number NKUIRB2025036) model was established, and cell counting, hematoxylin-eosin (HE) staining, and immunohistochemistry (IHC) detection of the tumor marker Ki67 confirmed that CPT suppressed PDO growth and malignant proliferation. A mouse xenograft tumor model was established (in compliance with the regulations of the Animal Ethics Committee of Tianjin University of Traditional Chinese Medicine, approval number: TCM-LAEC2025259K2011). Measurements of tumor volume and weight, HE staining, and Ki67 IHC demonstrated that CPT significantly inhibited tumor growth in vivo. Further studies found that a ferroptosis inhibitor could reverse the inhibitory effect of CPT on CRC cell proliferation, and CPT showed synergistic effects with ferroptosis inducers. Western blot and other detection results showed that CPT reduced the ratio of intracellular reduced glutathione (GSH) to oxidized glutathione (GSSG), and increased the levels of 4-hydroxynonenal (4-HNE) and the lipid peroxidation product malondialdehyde (MDA). Mechanistic studies indicated that CPT decreased glutathione peroxidase 4 (GPX4) mRNA levels and protein expression in a concentration-dependent manner. In conclusion, CPT can induce ferroptosis in CRC cells through GPX4, thereby inhibiting CRC cell proliferation and exerting anti-colorectal cancer effects.

, authors=Yi-chen KOU¹, Xin-ru ZHAI², Zhen-ting GUAN¹, Huan-ran SUN², Xiang-ling WANG¹, Chang-liang SHAN^{2, *}, Shuai ZHANG^{1, 3, *}, authorsList=Yi-chen KOU, Xin-ru ZHAI, Zhen-ting GUAN, Huan-ran SUN, Xiang-ling WANG, Chang-liang SHAN, Shuai ZHANG, authorCompany=null, correspAuthors=Chang-liang SHAN, Shuai ZHANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=Copyright ©2026 Acta Pharmaceutica Sinica. All rights reserved., 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=1308840560010555547, articleId=1308840556168573066, tenantId=1146029695717560320, journalId=1189982191388893191, language=CN, title=隐丹参酮通过GPX4诱导铁死亡抑制结直肠癌细胞增殖, columnId=1190335348896011050, journalTitle=药学学报, columnName=研究论文, runingTitle=null, highlight=null, articleAbstract=

本研究旨在探讨隐丹参酮(cryptotanshinone, CPT) 在体内外对结直肠癌(colorectal cancer, CRC) 的抑制作用, 并基于铁死亡探讨其可能的作用机制。对结直肠癌HCT116和HCT8细胞给予不同浓度CPT处理, 通过细胞计数和克隆形成实验以及Annexin V/PI染色法发现CPT显著抑制CRC细胞活力和增殖能力, 促进细胞凋亡; 构建CRC类器官模型(patient-derived organoid, PDO, 遵循南开大学生物医学伦理委员会规定, 批件号: NKUIRB2025036), 通过细胞计数、苏木精-伊红(hematoxylin-eosin, HE) 染色和肿瘤标志物Ki67的免疫组织化学(immunohistochemistry, IHC) 检测证实CPT抑制PDO的生长和恶性增殖; 建立小鼠移植瘤模型(遵循天津中医药大学动物伦理委员会规定, 批准号: TCM-LAEC2025259K2011), 通过检测肿瘤体积与质量、HE染色和Ki67的IHC证实CPT显著抑制体内肿瘤生长。进一步研究发现, 铁死亡抑制剂可以逆转CPT对CRC细胞增殖的抑制作用并且CPT与铁死亡诱导剂具有协同增效的作用。Western blot等检测结果显示CPT降低细胞内还原型谷胱甘肽(reduced glutathione, GSH) 和氧化型谷胱甘肽(oxidized glutathione, GSSG) 的比值, 升高4-羟基壬烯醛(4-hydroxynonenal, 4-HNE) 含量与脂质过氧化物丙二醛(malondialdehyde, MDA) 水平。机制研究表明, CPT呈浓度依赖性地降低谷胱甘肽过氧化物酶4 (glutathione peroxidase 4, GPX4) mRNA水平及蛋白表达。综上所述, CPT可通过GPX4诱导CRC细胞铁死亡, 从而抑制CRC细胞增殖, 发挥抗结直肠癌的作用。

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A, B: IC₅₀ of CPT in HCT116 (A) and HCT8 (B) cells; C, D: The growth curve of CPT in HCT116 (C) and HCT8 (D) cells; E, F: Colony formation assay of CPT in HCT116 (E) and HCT8 (F) cells. n = 3, x ± s. ^**P < 0.01, ^***P < 0.001, ^****P < 0.000 1. CPT: Cryptotanshinone, CRC: Colorectal cancer, figureFileSmall=yL9Ta4VJ18jmB5McukGoVw==, figureFileBig=VGFdIeM7zm7XjY9Jq2fz8Q==, tableContent=null), ArticleFig(id=1308840567958761689, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=EN, label=null, caption=null, figureFileSmall=NwllMJ+Ko0Q+5WzudgYDOA==, figureFileBig=qZ8fcAYGGWkaQ8kjXGSe0A==, tableContent=null), ArticleFig(id=1308840568025870554, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=CN, label=Fig.2, caption=Effect of CPT on CRC cell apoptosis. 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A: Representative images of CRC tumor-bearing model mice treated with the indicated doses of CPT; B: Tumor volume growth curves in mice treated with CPT; C: Representative images of excised tumors; D: Tumor weight at the end of the experiment. n = 5, x ± s. ^****P < 0.000 1, figureFileSmall=fj2x3Urrp1NoGkoIoWmJBw==, figureFileBig=BsvhJGBRQk0nVepujg6++Q==, tableContent=null), ArticleFig(id=1308840568373997791, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=EN, label=null, caption=null, figureFileSmall=HMJMPdt8SPZ1qBBAG9ulIA==, figureFileBig=JIsK+KokjPDCRW04UBmzfQ==, tableContent=null), ArticleFig(id=1308840568432718048, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=CN, label=Fig.5, caption=The effect of CPT on ferroptosis of CRC cell. A, B: Ferroptosis inhibitor DFO rescues the suppression of CPT on cell growth in HCT116 (A) and HCT8 (B) cells; C: Colony formation assay of CPT and DFO in HCT8 cells; D-G: Cell counting and colony formation assay of CPT and ferroptosis inducer erastin in CRC cells HCT116 (D and E) and HCT8 (F and G). n = 3, x ± s. ^**P < 0.01, ^***P < 0.001. DFO: Deferoxamine, figureFileSmall=HMJMPdt8SPZ1qBBAG9ulIA==, figureFileBig=JIsK+KokjPDCRW04UBmzfQ==, tableContent=null), ArticleFig(id=1308840568495632609, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=EN, label=null, caption=null, figureFileSmall=ogPPSXAr2czMbZWGfuIF8A==, figureFileBig=G5wUB2Im0HIN9BjFuN6v6w==, tableContent=null), ArticleFig(id=1308840568558547170, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=CN, label=Fig.6, caption=The effect of CPT on ferroptosis-related indicators in CRC cells. A, B: The polymer level of 4-HNE in HCT116 (A) and HCT8 (B) cells treated with the indicated doses of CPT; C, D: Statistical expression of MDA expression levels in HCT116 (C) and HCT8 (D) cells treated with the indicated doses of CPT; E: The level of LipROS in HCT116 cells under different concentrations of CPT; F, G: Statistical GSH level, GSSG level and GSH/GSSG ratio in CRC HCT116 (F) and HCT8 (G) cells. n = 3, x ± s. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001, ^****P < 0.000 1. 4-HNE: 4-Hydroxynonenal; MDA: Malondialdehyde; GSH: Reduced glutathione; GSSG: Oxidized glutathione, figureFileSmall=ogPPSXAr2czMbZWGfuIF8A==, figureFileBig=G5wUB2Im0HIN9BjFuN6v6w==, tableContent=null), ArticleFig(id=1308840568667599075, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=EN, label=null, caption=null, figureFileSmall=0BwuoVtiKjkpMeozaTIEVA==, figureFileBig=yMw+j6KZ6YGstq32p49MlQ==, tableContent=null), ArticleFig(id=1308840568730513636, tenantId=1146029695717560320, journalId=1189982191388893191, articleId=1308840556168573066, language=CN, label=Fig.7, caption=The mRNA and protein expression level of GPX4 in CRC cells. A, B: The mRNA expression level of GPX4 in HCT116 (A) and HCT8 (B) cells treated with different concentrations of CPT; C, D: The protein expression level of GPX4 in HCT116 (C) and HCT8 (D) cells treated with different concentrations of CPT. n = 3, x ± s. ^**P < 0.01, ^***P < 0.001, ^****P < 0.000 1. 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