Xu Mengxue,Qin Xinyue,Feng Jinzhou,Yan Weiping,Zhang Rongrong.Anti-inflammatory effect of autophagy in experimental autoimmune encephalomyelitis mice[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(16):1624-1628.
Xu Mengxue,Qin Xinyue,Feng Jinzhou,Yan Weiping,Zhang Rongrong.Anti-inflammatory effect of autophagy in experimental autoimmune encephalomyelitis mice[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(16):1624-1628.DOI:
Objective To explore the temporal variation of autophagy in C57BL/6 mice with experimental autoimmune encephalomyelitis (EAE) after immunization
and demonstrate its anti-inflammatory effect in EAE mice. Methods EAE models were established in 20 female C57BL/6 mice
and then the mice were killed in 3
7
16 and 30 d later for the expression of LC3B in the central nervous system (CNS) by Western blotting. Another 60 female C57BL/6 mice were randomly divided into the normal control group
EAE group and EAE+3-methyladenine (3-MA) group. Neurological function scores were performed to evaluate the neurological function. Immunohistochemical assay was performed to test the activation of microglia on the 7th day post immunization. Western blotting was employed to detect the expression of IL-1β in each group in 16 and 30 d after immunization. HE staining was used to observe the infiltration of inflammatory cells in the brain. Results ① The neural function was more seriously damaged in the EAE+3-MA group than the EAE group (P0.05). ② Western blot results showed the expression of LC3-II/LC-3I was decreased since 7 d post immunization (P0.05)
and then kept in a lower level compared to the normal group (P0.05). ③ There were activated microglia in 7 d post immunization (P0.05)
with more strongly activated cells in EAE+3-MA group (P0.05). ④ There were more infiltrated inflammatory cells in the EAE+3-MA group than the EAE group at the same time point (P0.05). ⑤ The expression of IL-1β was elevated in 16 and 30 d in the EAE group
which were more significantly in the EAE+3-MA group (P0.05). Conclusion Autophagy is decreased in the EAE mice
which may be the main cause for the pathogenesis of inflammation.