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首页|期刊导航|时珍国医国药|基于JAK/STAT信号通路探讨大黄灵仙方干预Th17/Treg细胞平衡缓解肝内胆管炎症的作用机制

基于JAK/STAT信号通路探讨大黄灵仙方干预Th17/Treg细胞平衡缓解肝内胆管炎症的作用机制

付军 刘萌 俞渊 庞浇安 张曼 陈伟棠 马天如 叶桂源 罗艳萍 韦慧怡

时珍国医国药2025,Vol.36Issue(9):1619-1626,8.
时珍国医国药2025,Vol.36Issue(9):1619-1626,8.DOI:10.70976/j.1008-0805.SZGYGY-2025-0904

基于JAK/STAT信号通路探讨大黄灵仙方干预Th17/Treg细胞平衡缓解肝内胆管炎症的作用机制

To explore the mechanism of Dahuang Lingxian Formula(大黄灵仙方)in intervening the Th17/Treg cell balance and relieving intrahepatic bile duct inflammation through regulating the JAK/STAT signaling pathway

付军 1刘萌 2俞渊 2庞浇安 2张曼 2陈伟棠 2马天如 3叶桂源 2罗艳萍 2韦慧怡2

作者信息

  • 1. 广西中医药大学第一附属医院,广西 南宁 530200||广西中医药大学,广西 南宁 530200
  • 2. 广西中医药大学第一附属医院,广西 南宁 530200
  • 3. 防城港市中医医院,广西 防城港 538000
  • 折叠

摘要

Abstract

Objective To explore the effect of Dahuang Lingxian Formula(大黄灵仙方,DHLXF)on the balance of Th17/Treg cell subsets in rats with intrahepatic bile duct inflammation via regulating the JAK/STAT signaling pathway.Methods 25 rats were randomly divided into the blank group,the model group,the Danning Tablet group,the DHLXF low-dose and high-dose groups,with 5 rats in each.Except for the blank group,the remaining groups were administered1.25 mg/kg lipopolysaccharide(LPS)to establish a rat model of intrahepatic bile duct inflammation.During modeling,the Danning tablet group(0.5 g/kg),and the DHLXF low-dose(2.4 g/kg)and high-dose(4.8 g/kg)groups were administered intragastrically,while the blank group and the model group were given an equal volume of normal saline.After 8 days,hematoxylin-eosin(HE)was used to observe the degree of pathological changes in the rat liver tissues.The microplate method and enzyme-linked immunosorbent assay(ELISA)were used to detect serum inflammatory factor levels(ALT,AST,TBil,DBil,TBA,JAK1,STAT1,Foxp3,IL-10,IL-17,TNF-α).Western blot(WB)and real-time fluorescence quantitative PCR(RT-qPCR)were used to detect the expression levels of JAK1,STAT1,Foxp3,RORγt protein and mRNA in the bile duct tissues.Flow cytometry was used to detect peripheral blood helper T cell 17(Th17)and regulatory T cell(Treg)levels,and calcu-late the Th17/Treg ratio.One-way analysis of variance was used for comparison of measurement data among multiple groups,and LSD-t test was used for further pairwise comparison.Results Compared with the model group,the bile duct structure of the rats in Danning tablet group and the DHLXF low-dose and high-dose groups was more regular and more complete.The depth of inflammatory infiltra-tion in the portal area was greatly improved,and cell necrosis and congestion were rarely seen.The overall pathological morphology re-covered well,and the expression of ALT,AST,TBil,DBil,TBA,JAK1,STAT1,IL-17,TNF-α in the serum and the protein and mRNA expression of JAK1,STAT1,RORγt were decreased,and the expression of Foxp3,IL-10 content and Foxp3 protein and mRNA expression increased,the number of Treg cells in the peripheral blood of rats increased,the number of Th17 cells decreased,and the Th17/Treg ratio decreased(P<0.05).Conclusion DHLXF inhibits Th17 cell proliferation and induces Treg cell differentiation by reg-ulating the JAK/STAT signaling pathway and the expression of related inflammatory factors,maintains the balance of Th17/Treg cell sub-populations,and reduces the inflammatory stress response of rat intrahepatic bile duct cells,and promotes the biliary tract to return to a non-inflammatory state,thereby preventing and treating intrahepatic bile duct stones.

关键词

大黄灵仙方/肝内胆管炎症/Janus 激酶/信号转导子与转录激活子/辅助性T细胞17/调节性T细胞

Key words

Dahuang Lingxian Formula(大黄灵仙方,DHLXF)/Intrahepatic bile duct inflammation/Janus kinase/signal trans-ducer and activator of transcription/Helper T cells 17/regulatory T cells

分类

医药卫生

引用本文复制引用

付军,刘萌,俞渊,庞浇安,张曼,陈伟棠,马天如,叶桂源,罗艳萍,韦慧怡..基于JAK/STAT信号通路探讨大黄灵仙方干预Th17/Treg细胞平衡缓解肝内胆管炎症的作用机制[J].时珍国医国药,2025,36(9):1619-1626,8.

基金项目

国家自然科学基金(82360889) (82360889)

第三批"岐黄工程"高层次人才团队培育项目(202411) (202411)

广西中医药大研究生教育创新计划项目(YCSY2023035) (YCSY2023035)

广西一流学科建设开放课题项目(2019XK062 ()

2019XK068) ()

广西中医药大学第一附属医院院级科研项目(2021QN001) (2021QN001)

广西中医药大学校级科研项目青年基金项目(2023QN008) (2023QN008)

时珍国医国药

OA北大核心

1008-0805

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