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基于网络药理学与实验验证探究阳和汤抑制乳腺癌的糖酵解机制

孙艾琳 李济宇 徐轶尔 孙贵才 范春香

山西医科大学学报2026,Vol.57Issue(8):845-856,12.
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山西医科大学学报2026,Vol.57Issue(8):845-856,12.DOI:10.13753/j.issn.1007-6611.2026.08.001

基于网络药理学与实验验证探究阳和汤抑制乳腺癌的糖酵解机制

Mechanism of Yanghe decoction in inhibiting breast cancer via glycolysis based on network pharmacology and experimental validation

孙艾琳 1李济宇 1徐轶尔 2孙贵才 3范春香1

作者信息

  • 1. 复旦大学附属浦东医院中医科,上海 201399
  • 2. 哈药集团技术中心
  • 3. 南昌大学第一附属医院骨科
  • 折叠

摘要

Abstract

Objective To investigate the potential mechanism of Yanghe decoction(YHT)in the treatment of triple-negative breast cancer.Methods ①Active components of YHT were screened using the TCMSP database,and disease targets were obtained from the GeneCards database.A component-target network was subsequently constructed,followed by molecular docking to validate the binding affinity between core components and key targets.②Sprague-Dawley(SD)rats were randomly divided into a control group and low-,medium-,and high-dose Yanghe Tang groups,which received intragastric administration of YHT at doses of 6,12,24 g/kg,respectively,twice daily(morning and evening)for 7 consecutive days.Blood samples were collected 1 h after the final administration,and sera were separated to obtain the corresponding medicated sera.MDA-MB-231 triple-negative breast cancer cells were then assigned to a control group(receiving 10%blank serum),and YHT low-,medium-,and high-dose groups(receiving 10%low-,medium-,and high-dose medicated serum,respectively).Cell proliferation viability was assessed by CCK-8 assay;cell migration and invasion were evaluated by Transwell assay;protein expression levels of E-Cadherin and N-Cadherin were detected by western blot;and glucose con-sumption and lactate production levels were also measured.③MDA-MB-231 cells were divided into a control group,a YHT high-dose group and a YHT high-dose+740Y-P(PI3K activator)group.Protein expression levels of p-PI3K,p-AKT,HIF-1α,HK2,and GLUT1 were examined by Western blot.Results ①Quercetin,neryl acetate,and oxyphenbutazone were identified as the core active compo-nents of YHT.Molecular docking demonstrated that these components exhibit favorable binding affinities for PI3K,AKT1,and HIF-1α proteins.②Compared with control group,the proliferation,migration,and invasion abilities of MDA-MB-231 triple-negative breast cancer cells significantly reduced in YHT low-,medium-,and high-dose groups(P<0.05);E-Cadherin expression was significantly up-regulated while N-Cadherin expression was significantly down-regulated(P<0.05);and glucose consumption and lactate production were markedly decreased(P<0.05).Moreover,compared with YHT low-and medium-dose groups,the above indicators in YHT high-dose group exhibited more pronounced changes(P<0.05).③Compared with control group,the protein expression levels of p-PI3K,p-AKT,HIF-1α,HK2,and GLUT1 in high-dose YHT group significantly decreased(all P<0.001).Compared with YHT high-dose group,protein levels of p-PI3K,p-AKT,HIF-1α,HK2,and GLUT1 significantly increased in YHT high-dose+740Y-P group(P<0.05).Conclusion YHT suppresses the migration,invasion,and epithelial-mesenchymal transition of triple-negative breast cancer cells and reduces the expression of glycolysis-related proteins,which may involve the inhibition of the PI3K/AKT/HIF-1α signaling axis.

关键词

阳和汤/三阴性乳腺癌/网络药理学/分子对接/上皮-间质转化/细胞生物学功能/PI3K/AKT信号通路/糖酵解

Key words

Yanghe decoction/triple-negative breast cancer/network pharmacology/molecular docking/epithelial-mesenchymal transition/cell biological function/PI3K/AKT signaling pathway/glycolysis

分类

医药卫生

引用本文复制引用

孙艾琳,李济宇,徐轶尔,孙贵才,范春香..基于网络药理学与实验验证探究阳和汤抑制乳腺癌的糖酵解机制[J].山西医科大学学报,2026,57(8):845-856,12.

基金项目

上海市浦东新区名中医工作室建设项目(PDZY-2025-0720) (PDZY-2025-0720)

上海市浦东新区名中医继承人培养项目(PDZY-2025-0949) (PDZY-2025-0949)

复旦大学附属浦东医院引进人才项目(YJYJRC202305) (YJYJRC202305)

国家自然科学基金项目(82260870) (82260870)

山西医科大学学报

1007-6611

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