盐酸阿比朵尔抗柯萨奇B_4病毒及免疫学机制的研究  

Study of arbidol hydrochloride's anti-coxsackie B4 virus activity and its immunological mechanisms

作　　者：张诗林[1] 吴迪[1] 薛枭[1] 张福明[2] 

机构地区：[1]吉林大学白求恩医学院,吉林长春130021 [2]吉林大学白求恩第一医院

出　　处：《中国地方病防治》2013年第5期330-332,共3页Chinese Journal of Control of Endemic Diseases

基　　金：吉林大学大学生创新创业训练计划项目(项目编号:2012A71189)

摘　　要：目的探讨盐酸阿比朵尔抗柯萨奇B4病毒的作用及其免疫学机制。方法以CoxsackieB4病毒感染BALB/c小鼠制备病毒感染性心肌炎模型,以低、中、高3个剂量(100、200、300 mg/kg)的盐酸阿比朵尔治疗7 d。ELISA法检测血清中细胞因子含量;荧光定量RT-PCR法检测心肌组织匀浆上清液中CoxsackieB4病毒载量以及小鼠脾脏组织匀浆上清液中转录因子T-bet和GATA3的基因表达。结果 ELISA检测结果表明,随着盐酸阿比朵尔治疗浓度的增加,小鼠血清中IFN-γ和GM-CSF的表达量逐渐升高,而IL-10的表达量逐渐下降;荧光定量RT-PCR法检测结果表明,盐酸阿比朵尔可以降低小鼠心肌组织中CoxsackieB4的病毒载量,可以下调GATA3的基因表达量,对T-bet基因表达量影响较弱。结论盐酸阿比朵尔具有明显的抗CoxsackieB4病毒的作用,其抗病毒机制与细胞因子的免疫调节以及维持Th1/Th2的动态平衡密切相关。Objective To study arbidol hydrochloride ’s immunological mechanism of its antiviral activity.Methods We use BALB / c mice to make virus infectious myocarditis model by infecting them with Coxsackie B4 virus.And use high,medium and low three doses（100 mg / kg,200 mg / kg,300 mg / kg） of arbidol hydrochloride to treat them for 7 days.ELISA method was used to detect the serum cytokines levels;fluorescence quantitative RT-PCR method was used to detect Coxsackie B4 viral load in myocardial tissue and mRNA expression of T-bet and GATA3 in the spleen tissue.Results ELISA test results showed that with the increase of concentration of arbidol hydrochloride,IFN-γ and GM-CSF expressing quantity increased,while the expression of IL-10 quantity gradually decreased in mice serum.The results of fluorescence quantitative RT-PCR method showed that arbidol hydrochloride could reduce Coxsackie B4 viral load in myocardial tissue of mice,and could down-regulated GATA3 gene expression,but its influence on gene expression of T-bet was weak.Conclusion Arbidol hydrochloride had a significant activity of anti-Coxsackie B4 virus,and its antiviral mechanism was related to the immunoregulation of cytokines and the dynamic equilibrium of Th1 / Th2.

关 键 词：盐酸阿比朵尔 CoxsackieB4病毒 病毒性感染 抗病毒机制 

分 类 号：R373.23[医药卫生—病原生物学]