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目的探讨地塞米松(DXM)对实验性自身免疫性脑脊髓炎(EAE)小鼠氧化应激水平及抗氧化酶系统的影响。方法应用髓鞘少突胶质细胞糖蛋白35-55(MOG35-55)诱导C57BL/6小鼠建立EAE模型。随机分为正常对照组、EAE组、DXM组,观察各组临床症状。于小鼠免疫后第13、20、30天,采用硫代巴比妥酸法检测脑组织MDA含量;应用免疫组织化学染色、免疫印迹法检测脑组织Nrf2、NADP(H)醌氧化还原酶1(NQO1)蛋白表达水平。结果 DXM组小鼠发病率、最高神经功能评分均显著低于EAE组(P<0.05)。免疫后各时间点,EAE组小鼠脑组织MDA含量较正常对照组明显增高(P<0.05);DXM组MDA含量较EAE组明显降低(P<0.05)。免疫后各时间点,EAE组和DXM组小鼠脑组织Nrf2、NQO1表达水平均较正常对照组明显增加(P<0.05);DXM组Nrf2、NQO1表达水平较EAE组明显增加(P<0.05),且Nrf2蛋白呈明显核内移现象。结论地塞米松减轻EAE小鼠氧化损伤的作用部分通过上调Nrf2表达、增加抗氧化酶水平而实现。
Objective To investigate the effects of dexamethasone (DXM) on oxidative stress and antioxidant enzyme system in experimental autoimmune encephalomyelitis (EAE) mice. Methods C57BL / 6 mice were induced by myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) to establish EAE model. Randomly divided into normal control group, EAE group, DXM group, to observe the clinical symptoms of each group. On the 13th, 20th and 30th days after the mice were immunized, the contents of MDA in the brain tissue were detected by thiobarbituric acid method. The expressions of Nrf2 and NADP (H) quinone oxidoreductase 1 in the brain tissues were detected by immunohistochemical staining and immunoblotting (NQO1) protein expression levels. Results The morbidity and the highest neurological score of mice in DXM group were significantly lower than those in EAE group (P <0.05). At each time point after immunization, the content of MDA in brain tissue of EAE group was significantly higher than that of normal control group (P <0.05). The content of MDA in DXM group was significantly lower than that in EAE group (P <0.05). At each time point after immunization, the expression levels of Nrf2 and NQO1 in brain tissue of EAE and DXM groups were significantly higher than those in normal control group (P <0.05); the expression levels of Nrf2 and NQO1 in DXM group were significantly higher than those in EAE group (P <0.05) , And Nrf2 protein showed obvious nuclear shift phenomenon. Conclusion The effect of dexamethasone on oxidative damage in EAE mice is partly achieved by up-regulating Nrf2 expression and increasing antioxidant enzyme level.