| Objective To explore the effect of ApoE on AMs and MMP-2 in the brain of mice with experimental autoimmune encephalomyelitis (EAE).Methods C57BL/6J ApoE-deficient (ApoE-/-) mice were defined as ApoE-/-Group. C57BL/6J mice were randomly divided into Wild-Type (WT) Group, Vehicle-Treated Group, Peptide-Treated Group and Normal Control Group. ApoE-/-Group,WT Group, Vehicle-Treated Group and Peptide-Treated Group were injected with MOG35-55 to induce EAE model. Score on mice symptoms. The inflammatory infiltration in the brain of each group was observed through Hematoxylin-Eosin staining. The expression of ICAM-1〠VCAM-1ã€NCAM-1 and MMP-2 were quantified by immunohistochemistry.Results Except Normal Control Group, inflammatory cells have different degrees of infiltration in different groups.Compared with Normal Control Group, the IOD/area of ICAM-1ã€VCAM-1ã€NCAM-1 and MMP-2 in the brain of mice in each group was significantly increased(P<0.05). The peak-symptom score and inflammatory cells infiltration of the brain in ApoE-/-Group were worse than those in WT Group. Besides, peptide treatment decreased the peak-symptom score and immune infiltration in the brain. Comparing the IOD/area of ICAM-1ã€VCAM-1ã€NCAM-1 and MMP-2,it indicates that ApoE-/-Group’s was significantly higher than WT Group’s(P<0.05), as well as Peptide-Treated Group’s was lower than Vehicle-Treated Group’s (P<0.05).Conclusions A lack of ApoE in could enhance inflammatory responses〠pathological damage and up-rgulate the expression of ICAM-1ã€VCAM-1〠NCAM-1 and MMP-2 in EAE, however, the ApoE mimetic peptide could ameliorate these pathological states.Thus, ApoE might play a protective role in EAE by regulating the expression of ICAM-1ã€VCAM-1ã€NCAM-1 and MMP-2. |