伪狂犬病病毒(PRV)感染小鼠三叉神经节对NF-κB信号通路的影响及其调控炎症因子分泌  

Effects of PRV-infected mouse trigeminal ganglion on NF-κB signaling pathway and its regulation of inflammatory factor secretion

作　　者：杨志刚[1] 汤德元[1] 曾智勇[1] 王彬[1] 黄涛[1] 晏仁潭 韩超逸 陈阊峥 罗柳 袁盛林 陈旭[1] 廖正波 YANG Zhigang;TANG Deyuan;ZENG Zhiyong;WANG Bin;HUANG Tao;YAN Rentan;HAN Chaoyi;CHEN Changzheng;LUO Liu;YUAN Shenglin;CHEN Xu;LIAO Zhengbo(College of Animal Science,Guizhou University,Guiyang 550025,China)

机构地区：[1]贵州大学、动物科学学院,贵州贵阳550025

出　　处：《中国兽医学报》2023年第1期115-122,共8页Chinese Journal of Veterinary Science

基　　金：国家自然科学基金资助项目(31860716);贵州省科技支撑计划资助项目(黔科合支撑[2017]2583);贵州省科技支撑计划资助项目(黔科合支撑[2021]一般162);贵州省科技计划资助项目(黔科合平台人才[2018]5781-8)。

摘　　要：为了探究伪狂犬病病毒(PRV)感染小鼠三叉神经节对NF-κB信号通路的影响及其调控炎症因子分泌的情况,本试验用105TCID50PRV滴鼻感染小鼠后使用实时荧光定量PCR(q-PCR)检测不同时间段MyD88、TRIF、NF-κB p65、IL-1β、IL-6和TNF-α基因的转录情况,Western blot检测不同时间段MyD88、TRIF、IκBα、NF-κB p65、p-IκBα和NF-κB p-p65的表达情况,ELISA检测不同时间段IL-1β、IL-6和TNF-α的表达情况。结果显示,PRV感染小鼠三叉神经节后在早期会下调MyD88、TRIF和NF-κB p65基因mRNA转录(P<0.01),晚期会上调MyD88、TRIF和NF-κB p65基因mRNA转录(P<0.01),总体来说呈现先下调后上调的总趋势;Western blot结果显示,PRV感染小鼠三叉神经节后诱导IκBα和NF-κB p65的磷酸化,而对MyD88和TRIF的蛋白表达呈现先下调后上调的趋势,IκBα和NF-κB p65的蛋白表达呈现先下调后上调再下调的趋势,结果与mRNA转录情况基本一致;RT-qPCR结果显示PRV感染小鼠三叉神经节后IL-1β和IL-6基因mRNA转录在前期无变化,在后期极显著上调(P<0.001),TNF-α基因mRNA转录无变化;ELISA结果显示,PRV感染小鼠三叉神经节后IL-6表达在前期无变化,在后期极显著上调(P<0.001),IL-1β和TNF-α表达无变化。说明PRV感染小鼠三叉神经节后会激活NF-κB信号通路和调控炎症因子分泌,该研究结果为深入阐明PRV感染小鼠三叉神经节的致病机制奠定基础。This study aims to explore the effect of PRV-infected mouse trigeminal ganglion on NF-κB signaling pathway and its regulation of inflammatory factor secretion.This experiment was based on mouse.After intranasal infection of mouse with 10~5 TCID50PRV,real-time quantitative PCR(q-PCR)was used to detect MyD88,TRIF,NF-κB p65,IL-1β,IL-6 and TNF-αgenes at different time periods.Western blot was used to detect the expression of MyD88,TRIF,IκBα,NF-κB p65,p-IκBαand NF-κB p-p65 in different time periods.ELISA was used to detect the expression of IL-1β,IL-6 and TNF-αin different time periods.The results showed that the mRNA transcription of MyD88,TRIF and NF-κB p65 gene was down-regulated in the early stage after PRV infection in the trigeminal ganglia of mouse(P<0.01),and the mRNA transcription of MyD88,TRIF and NF-κB p65 gene was up-regulated in the late stage(P<0.01),showing a general trend of first down-regulation and then up-regulation.Western blot results showed that PRV induced the phosphorylation of IκBαand NF-κB p65 in the trigeminal ganglia of mouse,while the protein expressions of MyD88 and TRIF were down-regulated first and then up-regulated.The protein expression of IκBαand NF-κB p65 showed a trend of first down-regulation,then up-regulation and then down-regulation,and the results were basically consistent with the mRNA transcription.RT-qPCR results showed that the mRNA transcription of the IL-1βand IL-6 genes in the trigeminal ganglia of PRV-infected mouse did not change in the early stage,but was significantly up-regulated in the later stage(P<0.001),and the TNF-αgene mRNA transcription did not change.ELISA results showed that the expression of IL-6 in the trigeminal ganglion of PRV-infected mouse did not change in the early stage.It was significantly up-regulated in the later stage(P<0.001),and the expressions of IL-1βand TNF-αremained unchanged,indicating that PRV infection of mouse trigeminal ganglia will activate the NF-κB signaling pathway and regulate the secretion of inflammat

关 键 词：伪狂犬病病毒(PRV) NF-ΚB 三叉神经节 炎症因子 

分 类 号：S852.65[农业科学—基础兽医学]