Xu Linxinyu, Yang Tianshu, Su Shaobo, Wang Fang
Department of Ophthalmology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai 200092, China.
Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Middle Yanchang Road, Shanghai 200092, China.
Biomed Res Int. 2016;2016:7948345. doi: 10.1155/2016/7948345. Epub 2016 May 8.
Purpose. To investigate the effect of 2-Methoxyestradiol (2ME2) on experimental autoimmune uveitis (EAU) and the mechanism. Method. C57BL/6 male mice were used to establish the EAU model. 2ME2 was abdominal administrated in D0-D13, D0-D6, and D7-D13 and control group was given vehicle from D0-D13. At D14, pathological severity was scored. Lymphocyte reaction was measured using MTT assay. T cell differentiation in draining lymph nodes and eye-infiltrating cells was tested by flow cytometry. Proinflammatory cytokines production from lymphocytes was determined by ELISA. Result. The disease scores from 2ME2 D0-D13, 2ME2 D0-D6, 2ME2 D7-D13, and vehicle groups were 0.20 ± 0.12, 1.42 ± 0.24, 2.25 ± 0.32, and 2.42 ± 0.24. Cells from all 2ME2 treated groups responded weaker than control (p < 0.05). The inhibitory effect of 2ME2 on lymphocyte proliferation attenuated from 2ME2 D0-D13 to 2ME2 D0-D6 and to 2ME2 D7-D13 groups (p < 0.05). 2ME2 treated mice developed fewer Th1 and Th17 cells both in draining lymph nodes and in eyes than control (p < 0.05). Lymphocytes from 2ME2 group secreted less IFN-γ and IL-17A than those from control (p < 0.05). Conclusion. 2ME2 ameliorated EAU progression and presented a better effect at priming phase. The possible mechanism could be the inhibitory impact on IRBP specific lymphocyte proliferation and Th1 and Th17 cell differentiation.
目的。探讨2-甲氧基雌二醇(2ME2)对实验性自身免疫性葡萄膜炎(EAU)的影响及其机制。方法。采用C57BL/6雄性小鼠建立EAU模型。在第0 - 13天、第0 - 6天和第7 - 13天对小鼠进行腹腔注射2ME2,对照组在第0 - 13天给予溶剂。在第14天,对病理严重程度进行评分。采用MTT法检测淋巴细胞反应。通过流式细胞术检测引流淋巴结和眼内浸润细胞中的T细胞分化。采用ELISA法测定淋巴细胞产生的促炎细胞因子。结果。2ME2第0 - 13天组、2ME2第0 - 6天组、2ME2第7 - 13天组和溶剂组的疾病评分分别为0.20±0.12、1.42±0.24、2.25±0.32和2.42±0.24。所有2ME2处理组的细胞反应均弱于对照组(p<0.05)。2ME2对淋巴细胞增殖的抑制作用从2ME2第0 - 13天组到2ME2第0 - 6天组再到2ME2第7 - 13天组逐渐减弱(p<0.05)。与对照组相比,2ME2处理的小鼠在引流淋巴结和眼中产生的Th1和Th17细胞较少(p<0.05)。2ME2组淋巴细胞分泌的IFN-γ和IL-17A低于对照组(p<0.05)。结论。2ME2改善了EAU的进展,在启动阶段效果更佳。可能的机制是对IRBP特异性淋巴细胞增殖以及Th1和Th17细胞分化的抑制作用。