柯里拉京对小鼠单纯疱疹病毒性脑炎Toll样受体3-干扰素诱导链接蛋白通路的调控机制研究  

Regulation Mechanism of Coliracin on Toll-Like Receptor 3-TIR Domain Containing Adaptor Inducing Interferon-βSignaling Pathway in Mice with Herpes Simplex Encephalitis

作　　者：王有琴 黄飞 张睿[1] 樊丽君 吴利利 吴安鹏 宁泽洋 林尧 王小菊[1] Wang Youqin;Huang Fei;Zhang Rui;Fan Lijun;Wu Lili;Wu Anpeng;Ning Zeyang;Lin Yao;Wang Xiaoju(Suizhou Central Hospital,Hubei Medical College,Hubei Suizhou 441300,China)

机构地区：[1]湖北医药学院附属随州市中心医院,湖北随州441300

出　　处：《儿科药学杂志》2021年第5期1-5,共5页Journal of Pediatric Pharmacy

摘　　要：目的:通过柯里拉京(Cor)干预单纯疱疹病毒性脑炎(HSE)小鼠模型,阐明柯里拉京对Toll样受体3(TLR3)信号通路的调控机制。方法:通过颅内注射单纯疱疹病毒1型(HSV1)建立单纯疱疹病毒性脑炎小鼠模型,每天定时灌胃1次等体积的柯里拉京或生理盐水,在第5天断头处死小鼠,取出右侧颞叶病变脑组织进行苏木精-伊红(HE)染色,在显微镜下观察小鼠脑组织病理改变,通过定时定量PCR检测TLR3及其下游信号分子TLR结构域的干扰素诱导链接蛋白(TRIF)mRNA的表达情况,Western blot检测TLR3、TRIF蛋白表达情况,ELISA法检测炎性组织细胞内干扰素α(IFN-α)的分泌情况。结果:HSE小鼠模型中TLR3及其下游分子TRIF的mRNA、蛋白表达及IFN-α的分泌均高于正常对照组(P<0.01);柯里拉京干预可有效缓解动物脑组织的病理变化,且TLR3及其下游分子TRIF的mRNA、蛋白表达及IFN-α的分泌均低于正常对照组(P<0.01)。结论:柯里拉京能明显抑制小鼠小胶质细胞内TLR3通路达到缓解单纯疱疹病毒1型引起的脑组织的损伤。Objective:To analyze the regulatory mechanism of Corilagin(Cor)on Toll-like receptor 3(TLR3)signaling pathway through the intervention of Cor in mice with herpes simplex encephalitis(HSE).Methods:The mice model of HSE was established by intracranial injection of herpes simplex virus 1(HSV1).The same volume of Cor or normal saline was given intragastrically at regular intervals every day.On the 5th day,the mice were decapitated and the right temporal lobe brain tissue was stained with hematoxylin-eosin(HE).The pathological changes of the brain tissue were observed by microscope.Real-Time PCR was used to detect the expression of TIR domain containing adaptor inducing interferon-β(TRIF)mRNA in TLR3 and its downstream signal molecule TLR domain.Western blot was used to detect the expression of TLR3 and TRIF.ELISA method was used to detect the secretion of interferonα(IFN-α)in cells of inflammatory tissues.Results:The mRNA and protein expression of TLR3 and its downstream molecule TRIF and the secretion of IFN-αin the mice model of HSE were higher than those in the normal control group(P<0.01).Intervention of Cor can effectively alleviate the pathological changes in animal brain tissues,the mRNA and protein expression of TLR3 and its downstream molecule TRIF and the secretion of IFN-αwere lower than those of the normal control group(P<0.01).Conclusion:Cor can significantly inhibit the TLR3 pathway in microglia of mice and alleviate the brain tissue damage induced by HSV1.

关 键 词：柯里拉京 单纯疱疹病毒1型 脑炎 Toll样受体3-干扰素诱导链接蛋白信号通路 

分 类 号：R512.3[医药卫生—内科学]