IL-17在急性神经炎症中的神经保护作用与机制
发布时间:2018-04-30 15:47
本文选题:IL- + 葡萄膜炎 ; 参考:《免疫学杂志》2015年07期
【摘要】:目的探讨IL-17参与急性神经炎症的神经保护作用与机制。方法用光感受器间维生素A类结合蛋白(interphotoreceptor retinoid binding protein,IRBP)免疫纯系Lewis大鼠,建立急性-单向型实验性自身免疫性葡萄膜炎(experimental autoimmune uveitis,EAU)模型。RT-PCR法检测在EAU进展中效应T细胞相关分子的表达,免疫荧光法检测视网膜内胶质纤维酸性蛋白(glial fibrillary acidic portein,GFAP)的表达。以PMA/Ionomycin刺激大鼠外周血单个核细胞产生的炎性上清模拟含高水平IL-17的炎性环境,ELISA法检测IL-17等细胞因子水平,Tunel法检测细胞凋亡。结果 EAU发病过程中视网膜局部呈现含高水平IL-17的炎性环境,其中星型胶质细胞高度活化。以炎性上清刺激可诱发原代培养的小脑神经元大量凋亡,加入活化后星型胶质细胞或上清则使凋亡显著降低。IL-17中和抗体可显著抑制炎性上清对神经元的保护作用。结论急性神经炎症中星型胶质细胞通过分泌IL-17发挥神经保护作用。
[Abstract]:Objective to investigate the neuroprotective effect and mechanism of IL-17 in acute neuritis. Methods the immunized pure Lewis rats were immunized with interphotoreceptor retinoid binding protein (IRBP), an acute unidirectional experimental autoimmune uveitis model. RT-PCR was used to detect the expression of effector T cell-related molecules in the progression of EAU. The expression of glial fibrillary acidic in retina was detected by immunofluorescence. The inflammatory supernatant produced by peripheral blood mononuclear cells (PBMC) stimulated by PMA/Ionomycin was used to simulate the inflammatory environment with high level of IL-17. The level of cytokines such as IL-17 was detected by Elisa and apoptosis was detected by Tunel method. Results the inflammatory environment with high level of IL-17 was present in the retina during the course of EAU, in which astrocytes were highly activated. The stimulation of inflammatory supernatant could induce a large number of apoptosis of primary cultured cerebellar neurons, and the addition of activated astrocytes or supernatants could significantly reduce the apoptosis. IL-17 neutralizing antibody could significantly inhibit the protective effect of inflammatory supernatant on neurons. Conclusion astrocytes play a neuroprotective role in acute neuritis by secreting IL-17.
【作者单位】: 齐齐哈尔医学院免疫教研室;
【基金】:齐齐哈尔市科技局社会发展项目(SFGG-201209)
【分类号】:R774.6
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