Article(id=1291404294041887554, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404284806030089, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.04.006, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1724342400000, receivedDateStr=2024-08-23, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824376831, onlineDateStr=2026-08-04, pubDate=1740672000000, pubDateStr=2025-02-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824376831, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824376831, creator=13701087609, updateTime=1785824376831, updator=13701087609, issue=Issue{id=1291404284806030089, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='4', pageStart='451', pageEnd='600', issueExtLink='null', onlineDate='null', pubDate='1740672000000', pubDateStr='2025-02-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824374629, creator='13701087609', updateTime=1785824374629, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=477, endPage=481, ext={EN=ArticleExt(id=1291404294436152131, articleId=1291404294041887554, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Study on the mechanism of deoxyelephantopin regulating the progression of non-small cell lung carcinoma, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the inhibitory effect of deoxyelephantopin on non-small cell lung cancer (NSCLC) and its potential mechanism.
Methods Human lung adenocarcinoma H1975 cells were randomly divided into control group (routine culture), experimental-L group (1.0 μmol·L-1 deoxyelephantopin), experimental-M group (2.0 μmol·L-1 deoxyelephantopin), experimental-H group (5.20 μmol·L-1 deoxyelephantopin), Vector group (transfected Vector plasmid +5.20 μmol·L-1 deoxyelephantopin), epidermal growth factor receptor (EGFR) group (transfected with EGFR plasmid+5.20 μmol·L-1 deoxyelephantopin). 5-ethynyl-2′-deoxyuridine(EdU) assay was used to detected cell proliferation; cell apoptosis were detected by TdT mediated dUDP nick end labeling(Tunel)and flow cytometry; Western blot assay was used to detect the proteins expression; and Transwell assay was used to detect cell migration and invasion.
Results The proliferation rates of cells in the control group and experimental-L, -M, -H groups were (40.64±2.70)%, (29.78±3.28)%, (23.59±1.98)% and (15.72±1.01)%, respectively; the rates of TUNEL-positive cells were (4.63±0.57)%, (10.18±0.88)%, (15.96±0.79)% and (24.73±3.70)%, respectively; the relative expression levels of phosphorylated epidermal growth factor receptor (p-EGFR) protein were 0.87±0.10, 0.60±0.05, 0.49±0.04 and 0.33±0.04, respectively. Comparisons between the experimental-L, -M, -H groups and the control group, as well as comparisons among the experimental-L, -M, -H groups, revealed statistically significant differences (all P<0.05). The relative expression levels of p-EGFR/EGFR protein in the control group, experimental-H group, Vector group, and EGFR group were 0.76±0.10, 0.49±0.07, 0.47±0.05 and 0.71±0.10, respectively; apoptosis rates were (4.11±0.39)%, (26.33±2.29)%, (25.40±1.58)% and (12.68±1.73)%, respectively; the number of migrating cells was 147.78±12.69, 87.11±9.65, 93.89±9.67 and 124.00±14.10, respectively. Statistical analysis showed significant differences in the above indices between the experimental-H group and the control group, as well as between the EGFR group and the Vector group (all P<0.05).
Conclusion Deoxyelephantopin can degrade EGFR, inhibit related signaling pathways, inhibit proliferation and metastasis of lung cancer cells, and induce apoptosis.
, authors=Cai-xia XI, Wen-xue TAO, Xue-mei LIU, Wen-jing ZHANG, Hai-hui ZHANG, Wen-bo ZHANG, authorsList=Cai-xia XI, Wen-xue TAO, Xue-mei LIU, Wen-jing ZHANG, Hai-hui ZHANG, Wen-bo ZHANG, authorCompany=null, correspAuthors=Cai-xia XI, 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=1291404294889136965, articleId=1291404294041887554, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=去氧地胆草素调控非小细胞肺癌进展的机制研究, 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 探讨去氧地胆草素对非小细胞肺癌（NSCLC）的抑制作用及其潜在作用机制。
方法 将人肺腺癌H1975细胞随机分为对照组（常规培养）、低剂量实验组（1.0 μmol·L-1去氧地胆草素）、中剂量实验组（2.0 μmol·L-1去氧地胆草素）、高剂量实验组（5.20 μmol·L-1去氧地胆草素）、Vector组（转染Vector质粒+5.20 μmol·L-1去氧地胆草素）、EGFR组（转染过表达EGFR质粒+5.20 μmol·L-1去氧地胆草素）。用5-乙炔基-2′-脱氧尿苷（EdU）实验检测细胞增殖情况，用原位末端转移酶标记法（Tunel）、流式细胞术实验检测细胞凋亡情况，用蛋白质印迹法实验检测相关蛋白的表达水平，用Transwell实验检测细胞迁移和侵袭情况。
结果 对照组和低、中、高剂量实验组细胞增殖率分别为（40.64±2.70）%、（29.78±3.28）%、（23.59±1.98）%和（15.72±1.01）%，Tunel阳性细胞率分别为（4.63±0.57）%、（10.18±0.88）%、（15.96±0.79）%和（24.73±3.70）%，磷酸化表皮生长因子受体（p-EGFR）蛋白相对表达水平分别为0.87±0.10、0.60±0.05、0.49±0.04和0.33±0.04，低、中、高剂量实验组的上述指标分别与对照组比较，低、中、高剂量组组间比较，在统计学上差异均有统计学意义（均P<0.05）。对照组、高剂量实验组、Vector组和EGFR组的p-EGFR/EGFR蛋白相对表达水平分别为0.76±0.10、0.49±0.07、0.47±0.05和0.71±0.10，细胞凋亡率分别为（4.11±0.39）%、（26.33±2.29）%、（25.40±1.58）%和（12.68±1.73）%，迁移细胞数分别为（147.78±12.69）、（87.11±9.65）、（93.89±9.67）和（124.00±14.10）个；高剂量实验组的上述指标与对照组比较，EGFR组的上述指标与Vector组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 去氧地胆草素可通过降解EGFR，抑制相关信号通路，抑制肺癌细胞增殖和转移，并诱导凋亡。
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席彩霞（1978-），女，硕士，主任医师，主要从事肺部肿瘤方面的临床诊疗工作
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