TRAF2在柯萨奇A组10型病毒感染细胞中的表达及作用  

Preliminary study on the role of TRAF2 in regulating the infection of coxsackievirus A10

作　　者：金翠宁 徐扬 成昕宇 全传松 李玉明 刘绍琼 JIN Cuining;XU Yang;CHENG Xinyu;QUAN Chuansong;LI Yuming;LIU Shaoqiong(Key Laboratory of Emerging Infectious Diseases in Universities of Shandong;School of Clinical and Basic Medicine Sciences(Institute of Basic Medical Sciences);School of Public Health and Health Management,Shandong First Medical University&Shandong Academy of Medical Sciences,Jinan 250117,China)

机构地区：[1]山东第一医科大学(山东省医学科学院)山东省高等学校新发传染病病因流行病学重点实验室,山东济南250117 [2]山东第一医科大学(山东省医学科学院)临床与基础医学院(基础医学研究所),山东济南250117 [3]山东第一医科大学(山东省医学科学院)公共卫生与健康管理学院,山东济南250117

出　　处：《山东第一医科大学(山东省医学科学院)学报》2025年第1期17-23,共7页Journal of Shandong First Medical University & Shandong Academy of Medical Sciences

基　　金：国家自然科学基金(32470157);山东省中医药科技项目(Q-2022139);山东省自然科学基金(ZR2021MC001);山东省大学生创新创业训练计划(S202410439048);山东第一医科大学(山东省医学科学院)临床-基础联合创新团队项目(202407)。

摘　　要：目的探讨TNF受体相关因子2(tumor necrosis factor receptor-associated factor 2,TRAF2)在柯萨奇A组10型病毒(coxsackievirus A10,CVA10)感染细胞模型和动物模型中的表达及其作用机制。方法将CVA10接种至非洲绿猴肾细胞(Vero细胞)构建细胞模型,通过实时荧光定量PCR技术和Western blot技术检测核因子κB(nuclear factor kappa-B,NF-κB)和TRAF2的表达水平;通过TRAF2过表达的CVA10感染细胞模型进一步验证其相互作用。同时,收集不同日龄ICR小鼠血液样本,检测TRAF2的表达;构建ICR小鼠CVA10感染模型,分析CVA10感染后,不同时间点的血清中TRAF2的含量变化。结果研究发现,CVA10感染细胞后,TRAF2的表达显著下降,NF-κB的磷酸化和总蛋白的水平明显提高;而在TRAF2过表达细胞模型中,CVA10的复制受到抑制,NF-κB的磷酸化和总蛋白的水平显著下降。正常小鼠在不同日龄血清中TRAF2的表达存在差异,从5天到8周龄呈现先上升后下降的趋势,而在CVA10感染小鼠模型中,同样发现TRAF2的表达显著下调。结论CVA10感染可激活NF-κB信号通路,而TRAF2通过NF-κB信号通路来参与调控CVA10病毒复制、感染细胞的过程。Objective:This study aims to investigate the expression of tumor necrosis factor receptor-associated factor 2(TRAF2)and its mechanism of action in coxsackievirus A10(CVA10)infected cell and animal models.Methods:CVA10 was inoculated into African green monkey kidney cells(Vero)to construct the cell model,in which the expression of TRAF2 and NF-κB were detected by quantitative real-time PCR(qRT-PCR)and Western blotting.In addition,a CVA10 infected cell model with the overexpression of TRAF2 was built to verify their interaction further.Meanwhile,blood samples from ICR mice in different ages were collected to detect the expression of TRAF2.And,a CVA10 infected mouse model composed of ICR mice was constructed to analyze the changes of TRAF2 content in serum at different time sites after CVA10 infection.Results:In CVA10 infected cell model,the result shows that the expression of TRAF2 was significantly decreased,while the phosphorylation of NF-κB and the level of total protein were increased obviously.In TRAF2 overexpression cell model,the phosphorylation of NF-κB and the level of TP were decreased eminently,with the replication of CVA10 inhibited.The contents of TRAF2 in serum were varied in normal mice at different ages,showing a trend of increasing firstly and then decreasing from 5 days to 8 weeks.Compared to the control group,a significant down-regulation of TRAF2 expression in CVA10 infected mouse model was observed as well.Conclusion:The NF-κB pathway was activated by CVA10 infection,through which TRAF2 regulated the process of CVA10 infection and replication.

关 键 词：TNF受体相关因子2 柯萨奇A组10型病毒 病毒复制 核转录因子KB 感染模型 

分 类 号：R373[医药卫生—病原生物学]