基于NF-κB信号通路探讨鼻渊合剂对急性鼻窦炎的作用机制

Study on the Mechanism of Biyuan Heji in the Treatment of Acute Sinusitis Based on NF-κB Signal Pathway

目的基于NF-κB信号通路探讨鼻渊合剂对急性鼻窦炎的作用机制。方法通过中药系统药理学技术平台(TCMSP)及Uniprot数据库,筛选出鼻渊合剂中各药物的有效活性成分和对应靶基因。借助人类基因数据库(GeneCards)筛选出急性鼻窦炎相关的作用靶基因,取两靶基因的交集。使用生信在线分析全能网站(Metascape)进行基因本体功能富集分析(GO)和京都基因与基因组百科全书通路分析(KEGG)。利用Cytoscape软件构建“药物-活性成分-靶点”网络图,以及应用插件“Bisogenet”创建蛋白-蛋白互作(PPI)网络并进行数据分析。同时展开动物实验验证NF-κB信号通路。结果筛选出鼻渊合剂有效成分66个和对应靶基因239个,急性鼻窦炎相关靶基因2236个,交集基因141个,主要有效活性成分为槲皮素、山柰酚、β-谷甾醇等。GO和KEGG提示鼻渊合剂通过NF-κB信号通路、癌症途径、TNF信号通路等对急性鼻窦炎起作用。动物实验中急性鼻窦炎模型大鼠在灌胃鼻渊合剂后,体内NF-κB信号通路相关IL-1β、IL-6、IL-8、TNF-α、NF-κBp50、NF-κBp65的表达水平均有不同程度的下降。结论鼻渊合剂可改善急性鼻窦炎模型大鼠的炎症反应,其机制与干预NF-κB信号通路表达有关。

OBJECTIVE Based on NF-κB signaling pathway to explore the mechanism of Biyuan Heji(BYHJ)in The Treatment of Acute Sinusitis.METHODS Through TCMSP and Uniprot database,the effective active components and corresponding target genes of each drug in BYHJ were obtained.With the help of Genecards,the target genes related to acute sinusitis(ARS),and the intersection of the two target genes were retrieved.Metascape for GO and KEGG data was used.Cytoscape software was used to construct the network diagram of"Drug-Active ingredient-Target",and the plug-in,"Bisogenet",was used to create PPI network and analyze the imformation.At the same time,animal experiments were carried out to verify NF-κB signaling pathway.RESULTS 66 active components and 239 corresponding target genes of BYHJ,2236 target genes related to ARS and 141 intersection genes.The main active components were quercetin,kaempferol,β-sitosterol,etc.GO and KEGG suggested that BYHJ cured ARS via NF-κB signaling pathway,cancer pathway and TNF signaling pathway and so forth.In animal experiments,after gavage administration of BYHJ,the level of IL-1β、IL-6、IL-8、TNF-α、NF-κBp50、NF-κBp65,related to NF-κB signaling pathway,decreased in vary degrees in ARS rats.CONCLUSION BYHJ can reduce the inflammatory response of ARS rats,and its mechanism is to intervene NF-κB signaling pathway by inhibiting the expression of inflammatory factors.