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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 investigate the effect of cannabinoid 1 receptor (CB1R) overexpression on the neurological function in experimental autoimmune encephalomyelitis (EAE) mice and its mechanism. Methods Twenty-four C57B / L6 mice were selected and induced by MOG_ (35-55) immunization. The mice were randomly divided into 2 groups. One group was overexpression of CB1R in the spinal cord of mice by plasmid transfection, Solvents were given as a control. The neurological deficit in EAE mice in control group and CB1R overexpression group was observed. The expression of CB1R protein in spinal cord of mice was detected by Western blotting. The levels of cytokines interleukin (IL) in mice spinal cord were detected by enzyme-linked immunosorbent assay (ELISA) -10, IL-17, IL-6, and tumor necrosis factor alpha (TNF-alpha). Results At the 14th and 28th days after immunization, the extent of neurological deficit in EAE mice with CB1R overexpression group was lower than that in the control group (P <0.05). Compared with the control group, the expression of CB1R protein in CB1R-overexpressed EAE mice increased (P <0.01) and the concentration of IL-10 increased (P <0.05), while the levels of IL-17 and IL-6 , The concentration of TNF-α decreased (P <0.05, P <0.01). Conclusion Overexpression of CB1R in central nervous system can delay the occurrence and development of EAE. This effect may be achieved through immunomodulation.