Article(id=1291704930616763089, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.18.012, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1740067200000, receivedDateStr=2025-02-21, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785896054175, onlineDateStr=2026-08-05, pubDate=1758988800000, pubDateStr=2025-09-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785896054175, onlineIssueDateStr=2026-08-05, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785896054175, creator=13701087609, updateTime=1785896054175, updator=13701087609, issue=Issue{id=1291704811443999077, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='18', pageStart='2551', pageEnd='2700', issueExtLink='null', onlineDate='null', pubDate='1758988800000', pubDateStr='2025-09-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785896025763, creator='13701087609', updateTime=1785896871490, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291708358743053253, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291708358743053254, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291704811443999077, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=2639, endPage=2644, ext={EN=ArticleExt(id=1291704931321406162, articleId=1291704930616763089, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Mechanism study on the angiogenesis of colitis-associated colon cancer intervened by Hedysari Radix Paeparata Cum Melle -vinegar processed Curcumae Rhizoma, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To explore the mechanism by which processed Radix Hedysari and vinegar-processed Rhizoma Curcumae inhibit angiogenesis in colitis-associated colorectal cancer (CAC).
Methods Sixty SPF-grade C57BL/6J mice were randomly divided into six groups (A-F), A: Blank control; B: Model group [Azoxymethane (AOM)/Dextran sodium sulfate (DSS) AOM/DSS group]; C: Sulfasalazine group; D: Fried Astragalus group; E: Fried Astragalus-Vinegar Curcuma (4∶1) group; F: Curcuma zedoaria group. Each group contained 10 mice. A CAC mouse model was induced using combined AOM and DSS. Simultaneously, each treatment group received intervention, the blank group received 0.9% sodium chloride solution. The experiment concluded after 17 weeks of intervention. Collagen fiber area expression in colon tissues was assessed using Masson’s trichrome staining. Microvascular density in colon tissues was determined via immunohistochemistry. Serum vascular endothelial growth factor(VEGF) and nitric oxide(NO) levels were measured using enzyme linked immunosorbent assay(ELISA). Key proteins in the phosphatidylinositol-3-kinase/ protein kinase B(PI3K/AKT) pathway and VEGF expression were detected by Western blotting (WB).
Results After 17 weeks of pharmacological intervention, the microvessel counts in the blank group, model group, sulfasalazine group, honey-fried Radix Hedysari-vinegar-processed Rhizoma Curcumae (4:1) group, honey-fried Radix Hedysari group, and vinegar-processed Rhizoma Curcumae group were (23.20±4.21), (73.60±13.52), (44.80±2.78), (33.40±6.31), (41.60±3.36), and (47.80±7.29), respectively. The serum VEGF concentrations were (83.03±24.13), (153.61±18.69), (115.08±11.43), (87.03±25.24), (91.33±32.37), and (101.93±19.74) pg·mL-1, respectively. The serum NO levels were (28.46±5.91), (40.62±2.28), (30.62±6.54), (29.18±5.37), (30.87±5.30), and (32.29±3.43) μmol·L-1, respectively. Compared with the blank group, the model group exhibited significant increases in the collagen fiber staining area and microvessel density in colonic tissue, markedly elevated serum VEGF and NO levels, and significantly enhanced phosphorylation of PI3K, AKT, and mTOR as well as upregulated VEGF expression in colonic tissue. In comparison with the model group, the honey-fried Radix Hedysari-vinegar-processed Rhizoma Curcumae (4∶1) group, honey-fried Radix Hedysari group, and vinegar-processed Rhizoma Curcumae group demonstrated significant reductions in the collagen fiber area and microvessel count in colonic tissue, decreased serum VEGF and NO concentrations, and markedly suppressed phosphorylation of PI3K, AKT, and mTOR along with downregulated VEGF expression in colonic tissue (P<0.05 or P<0.01).
Conclusion The combined use of processed Radix Hedysari and vinegar-processed Rhizoma Curcumae exerts a better anti-CAC effect than the single herb. Its mechanism is closely related to regulating the expressions of key proteins in the PI3K/AKT signaling pathway, thereby inhibiting angiogenesis in colitis-associated colorectal cancer.
, authors=Ting LIU
1, 2, Rui-long LÜ
1, 2, Zhuan-hong ZHANG
1, 2, Yu-gui ZHANG
2, Ding-cai MA
1, 2, Er-dan XIN
1, 2, Yu-jing SUN
2, Fen-yu DOU
1, 2, Meng-na CHAI
1, 2, Yue-feng LI
2, authorsList=Ting LIU, Rui-long LÜ, Zhuan-hong ZHANG, Yu-gui ZHANG, Ding-cai MA, Er-dan XIN, Yu-jing SUN, Fen-yu DOU, Meng-na CHAI, Yue-feng LI, authorCompany=null, correspAuthors=Yue-feng 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=1291704932164461267, articleId=1291704930616763089, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=炙红芪-醋莪术干预结肠炎相关结肠癌血管生成的机制研究, 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 探讨炙红芪-醋莪术抑制结肠炎相关结肠癌血管生成的作用机制。
方法 将60只SPF级C57BL/6J小鼠随机分为A~F 6组,分别是A:空白组;B:模型组[氧化偶氮甲烷(AOM)/葡聚糖硫酸钠(DSS),AOM/DSS组];C:柳氮磺胺吡啶组;D:炙红芪组;E:炙红芪-醋莪术(4∶1)组;F:醋莪术组,每组10只。用AOM与DSS联合诱导结肠炎相关结直肠癌(CAC)小鼠模型的同时,各组给药干预,空白组给予0.9%NaCl溶液,干预17周后实验结束。用Masson染色法观察各组小鼠结肠组织中胶原纤维面积的表达;用免疫组化法测定各组小鼠结肠组织中微血管密度;使用酶联免疫吸附试验(ELISA)法测定各组小鼠血清中血管内皮生长因子(VEGF)及一氧化氮(NO)的表达;用蛋白免疫印迹法(WB)检测磷脂酰肌醇3激酶/蛋白激酶B(PI3K/AKT)通路关键蛋白及VEGF表达。
结果 在药物干预治疗17周后,空白组、模型组、柳氮磺胺吡啶组、炙红芪-醋莪术(4∶1)组、炙红芪组及醋莪术组的微血管数量分别为(23.20±4.21)、(73.60±13.52)、(44.80±2.78)、(33.40±6.31)、(41.60±3.36)和(47.80±7.29)个,血清中VEGF的含量分别为(83.03±24.13)、(153.61±18.69)、(115.08±11.43)、(87.03±25.24)、(91.33±32.37)和(101.93±19.74)pg·mL-1,血清中NO的含量分别为(28.46±5.91)、(40.62±2.28)、(30.62±6.54)、(29.18±5.37)、(30.87±5.30)和(32.29±3.43)μmoL·L-1。与空白组相比,模型组小鼠结肠组织中胶原纤维染色面积、微血管数量显著增加,血清中VEGF、NO含量显著上升,结肠组织中PI3K、AKT、mTOR磷酸化表达及VEGF的表达显著升高;与模型组比较,炙红芪-醋莪术(4∶1)组、炙红芪组及醋莪术组小鼠结肠组织中胶原纤维面积及微血管数量显著减少,血清中VEGF、NO含量均有所降低,结肠组织中PI3K、AKT、mTOR的磷酸化表达及VEGF的表达明显降低(P<0.05或P<0.01)。
结论 炙红芪-醋莪术配伍抗结肠炎相关结肠癌的作用优于单味药,其作用机制与炙红芪-醋莪术通过调控PI3K/AKT信号通路关键蛋白的表达,抑制结肠炎相关结肠癌的血管生成密切相关。
, authors=刘婷
1, 2, 吕瑞龙
1, 2, 张转红
1, 2, 张育贵
2, 马定财
1, 2, 辛二旦
1, 2, 孙宇靖
2, 窦芬瑜
1, 2, 柴梦娜
1, 2, 李越峰
2, authorsList=刘婷, 吕瑞龙, 张转红, 张育贵, 马定财, 辛二旦, 孙宇靖, 窦芬瑜, 柴梦娜, 李越峰, authorCompany=null, correspAuthors=李越峰, authorNote=
刘婷(1999-),女,博士研究生在读,主要从事中药及复方加工炮制机制及活性成分研究
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1.College of Pharmacy, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
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1.甘肃中医药大学 药学院,甘肃 兰州 730000
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刘婷(1999-),女,博士研究生在读,主要从事中药及复方加工炮制机制及活性成分研究
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1.College of Pharmacy, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
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1.甘肃中医药大学 药学院,甘肃 兰州 730000
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1.College of Pharmacy, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu Province, China
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1.甘肃中医药大学 药学院,甘肃 兰州 730000
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