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过敏煎治疗特应性皮炎的作用机制:基于网络药理学和分子对接技术OA

Mechanisms of Guomin Decoction in the treatment of atopic dermatitis:Based on network pharmacology and molecular docking

中文摘要英文摘要

目的 运用网络药理学方法,探究过敏煎治疗特应性皮炎(AD)的可能机制,并通过细胞实验验证其核心成分的调控作用.方法 用TCMSP及相关文献资料检索过敏煎有效成分和作用靶点,利用OMIM和Genecards数据库检索OP的相关靶点.获取交集靶点并导入String数据库进行蛋白互作处理,筛选核心靶点,并利用Cytoscape软件对其进行可视化.通过组胺诱导HaCaT细胞构建AD细胞模型,设置1 μmol/L、5 μmol/L浓度槲皮素干预组、山柰酚干预组,采用ELISA法检测细胞上清中TNF-α、IL-1β含量,RT-PCR法检测STAT3、MAPK1 mRNA表达水平,验证核心成分的作用.结果 用Cyto-scape 的cytohubba插件对核心靶点进行GO和KEGG富集分析.共筛选出过敏煎活性成分36个,对应药物靶点1 161个;获取AD疾病靶点1 780个,最终得到药物-疾病交集靶点383个.PP网络分析结合cytohubba插件筛选出STAT3、MAPK1、RELA、JUN、MAPK8、TNF等核心靶点;GO富集分析显示核心靶点主要参与"炎症反应""MAPK级联反应调控"等生物学过程,KEGG富集分析明确其显著富集于TNF信号通路、JAK-STAT信号通路、MAPK信号通路、IL-17信号通路等10条关键通路.细胞实验结果显示:与AD模型组相比,5 μmol/L浓度槲皮素、山柰酚组可显著降低细胞上清中TNF-α、IL-1β含量(P<0.01),同时显著下调核心靶点STAT3、MAPK1的mRNA表达水平(P<0.05),有效抑制AD细胞模型的炎症反应.结论 过敏煎通过36个活性成分作用于383个疾病交集靶点,调控TNF、JAK-STAT等10条关键通路;核心成分槲皮素、山柰酚可显著降低AD细胞模型中TNF-α、IL-1β含量,下调STAT3、MAPK1 mRNA表达水平,有效抑制炎症反应.

Objective To investigate the potential mechanisms of Guomin Decoction(GMD)in the treatment of atopic dermatitis(AD)using network pharmacology,and to verify the regulato-ry effects of its core components in cell cultures.Methods The active components and corre-sponding targets of GMD were retrieved from TCMSP and relevant literature.Targets related to AD were obtained from OMIM and Genecards databases.Common targets were identified and imported into the String database for protein-protein interaction(PPI)analysis to screen core targets,which were then visualized using Cytoscape software.A cell model of AD was established by treating HaCaT cells with histamine.Intervention groups were treated with quercetin and kaempferol at dif-ferent concentrations(1 μmol/L,5 μmol/L).The levels of TNF-α and IL-1 β in cell superna-tants were detected by ELISA,and the mRNA expression levels of STAT3 and MAPK1 were meas-ured by RT-PCR to verify the effects of the core components.Results A total of 36 active compo-nents of GMD were identified,corresponding to 1 161 drug targets.A total of 1 780 AD-related disease targets were obtained,and 383 drug-disease common targets were finally determined.PPI network analysis combined with the Cytohubba plugin screened out core targets,including STAT3,MAPK1,RELA,JUN,MAPK8,and TNF-α.GO enrichment analysis showed that the core tar-gets were mainly involved in biological processes such as"inflammatory response"and"regulation of MAPK cascade reaction".KEGG enrichment analysis confirmed that these targets were signifi-cantly enriched in 10 key pathways,including the TNF signaling pathway,JAK-STAT signaling pathway,MAPK signaling pathway,and IL-17 signaling pathway.The results of cell cultures showed that,compared with the AD model group,the quercetin and kaempferol(at 5 μmol/L)significantly reduced the levels of TNF-α and IL-1 β in the supernatants(P<0.01)and downreg-ulated the mRNA expression levels of the core targets' STAT3 and MAPK1(P<0.05),effective-ly inhibiting the inflammatory response in the cell model of AD.Conclusions GMD acts on 383 common disease targets through 36 active components to regulate 10 key pathways,such as those involving TNF and JAK-STAT.Its core components,quercetin and kaempferol,can significantly reduce the levels of TNF-α and IL-1β and downregulate the mRNA expression of STAT3 and MAPK1 in the cell model of AD,thereby effectively inhibiting the inflammatory response.

王圣鑫;谢碧香;杨洋;谢凯

南方医科大学皮肤病医院,广东 广州 510000南方医科大学皮肤病医院,广东 广州 510000南方医科大学皮肤病医院,广东 广州 510000南方医科大学皮肤病医院,广东 广州 510000

特应性皮炎过敏煎网络药理信号通路

atopic dermatitisGuomin Decoctionnetwork pharmacologysignaling path-way

《皮肤性病诊疗学杂志》 2026 (2)

92-101,10

医药临床与成果转化基金-临床药学发展科研基金(Z-2014-08-2309-10)

10.3969/j.issn.1674-8468.2026.02.003

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