大麻素1型受体过表达在实验性自身免疫性脑脊髓炎小鼠中的作用  

Effect of cannabinoid 1 receptor overexpression on mice with experimental autoimmune encephalomyelitis

作　　者：程洁[1] 李琳[1] 楼之茵[1] 赵忠新[2] 

机构地区：[1]上海交通大学医学院附属新华医院神经内科,上海200092 [2]第二军医大学长征医院神经内科,上海200003

出　　处：《第二军医大学学报》2017年第3期345-348,共4页Academic Journal of Second Military Medical University

基　　金：国家自然科学青年基金(81200921)~~

摘　　要：目的探讨大麻素1型受体(cannabinoid 1receptor,CB1R)过表达对实验性自身免疫性脑脊髓炎(experimental autoimmune encephalomyelitis,EAE)小鼠神经功能的影响及其作用机制。方法选取24只C57B/L6小鼠,采用MOG_(35-55)免疫诱导构建EAE小鼠模型,随机分为2组,一组采用质粒转染技术使小鼠脊髓组织CB1R过表达,另一组给予溶剂作为对照。观察对照组和CB1R过表达组EAE小鼠的神经功能缺损症状,采用蛋白质印迹法检测小鼠脊髓组织中CB1R蛋白的表达,采用酶联免疫吸附试验检测小鼠脊髓组织中细胞因子白介素(IL)-10、IL-17、IL-6、肿瘤坏死因子α(TNF-α)的浓度。结果免疫后第14、28天时CB1R过表达组EAE小鼠发生神经功能缺损的程度低于对照组(P<0.05)。与对照组相比,CB1R过表达组EAE小鼠脊髓组织中CB1R蛋白的表达水平升高(P<0.01),IL-10的浓度升高(P<0.05),而IL-17、IL-6、TNF-α的浓度降低(P<0.05,P<0.01)。结论中枢神经细胞中CB1R的过表达能够延缓EAE的发生和发展,这种作用可能是通过免疫调节实现的。Objective To explore the effect of cannabinoid 1receptor（CB1R）overexpression on the neurological function of mice with experimental autoimmune encephalomyelitis（EAE）and the related mechanism. Methods Twenty-four C57B/L6 mice were selected to prepare EAE models by MOG35-55 immunization and were divided into two groups.CB1 R was overexpressed in mouse spinal cord tissue by plasmid transfection technique in CB1 Roverexpression group,and the other group was given solvent as control.The neurological deficits of mice were observed in control group and CB1 Roverexpression group.The expression of CB1 Rin the spinal cord of mice were detected by Western blotting analysis.The concentrations of interleukin（IL）-10,IL-17,IL-6,and tumor necrosis factor-α（TNF-α）were measured by ELISA.Results The degree of neurological deficit of mice in the CB1 Roverexpression group was significantly lower than that in the control group on 14 th and 28 th day after immunization（P〈0.05）.Compared with the control group,the expression of CB1 Rprotein in spinal cord in the CB1 Roverexpressing group was significantly increased（P〈0.01）,the concentration of IL-10 was significantly increased（P〈0.05）,and the concentrations of IL-17,IL-6,and TNF-αwere significantly decreased（P〈0.05,P〈0.01）.Conclusion CB1 R overexpression in central nervous cells can postpone the development and progression of EAE in mice,which may be achieved through immuomodulation.

关 键 词：CB1大麻酚受体 实验性自身免疫性脑脊髓炎 白介素类 肿瘤坏死因子Α 

分 类 号：R744.5[医药卫生—神经病学与精神病学]