Effect Of Apolipoprotein E On Inflammation In Mice With Experimental Autoimmune Encephalomyelitis

Objective To explore the effect of Apolipoprotein E(ApoE) on cytokine in central nervous system of mice with experimental autoimmune encephalomyelitis (EAE).Methods C57BL/6J apolipoprotein E-deficient (ApoE-/-) mice were used as ApoE-/- group.For the experiments, C57BL/6J mice were randomly divided into wild-type(WT) group, peptide-treated group,vehicle-treated group and normal control group. ApoE-/- group,WT group, peptide-treated group and vehicle-treated group were injected with MOG35-55 to induce EAE model. Score on mice symptoms.The inflammatory infiltration in the spinal cord of each group was observed through H-E staining. The expression of IL-17,IL-6 and TNF-a were quantified by immunohistochemistry.The expression of IL-6 and TNF-a were assayed by ELISA.Results Except the control group, inflammatory cells of EAE mice in different groups have different degrees of infiltration.Compared with the control group, the IOD/area of IL-17,IL-6 and TNF-a in the brain and spinal cord of mice in each group were significantly increased.The peak symptoms score and spinal inflammatory cells infiltration in ApoE-/- group were worse than those in WT group,and peptide treatment decreased the peak symptoms score and immune infiltration in spinal cord. Comparing the IOD/area of IL-17,IL-6 and TNF-a indicates that the ApoE-/- group’s was significantly higher than the WT group’s(P<0.05),as well as the Peptide-treated group was lower than the vehicle-treated group(P<0.05).Conclusion The expression of IL-17,IL-6 and TNF-a increased in the EAE mice.ApoE deficiency in the EAE could enhance inflammatory infiltrates into theCNS,and increase the level of IL-17,IL-6 and TNF-a. The ApoE mimetic peptide can inhibit the expression of IL-17,IL-6 and TNF-a.ApoE may play a protective role in EAE by regulating the expression of IL-17,IL-6 and TNF-a.