RESUMO
OBJECTIVE@#To detect the expression of macrophage migration inhibitory factor(MIF) in the brain and spinal cord of chronic non-remitting model of experimental autoimmune encephalomyelitis(EAE) mouse, and to discuss their effect on EAE/MS.@*METHODS@#Seventy-two female SPF C57BL/6J mice, aged 6k8 weeks, were randomly divided into an EAE group, a blank group, and an adjuvant group. The mice were immuned by mMOG35-55 and CFA. Immunohistochemic technique was used to detect the expression of MIF in the brain and spinal cord.@*RESULTS@#In the EAE group, we observed up-regulation of MIF of central nervous system(CNS) at onset, peak and chronic phase. During each phase, the difference of MIF between the EAE group and each of the other 2 groups was significant (P<0.05). In the EAE group, the expression of MIF was the highest at the peak, which was different from other periods (P<0.05).@*CONCLUSION@#MIF significanty expressed during the procedure of EAE disease, and may be related with the onset and exacerbation of EAE.
Assuntos
Animais , Feminino , Camundongos , Encéfalo , Metabolismo , Modelos Animais de Doenças , Encefalomielite Autoimune Experimental , Metabolismo , Fatores Inibidores da Migração de Macrófagos , Camundongos Endogâmicos C57BL , Distribuição Aleatória , Regulação para CimaRESUMO
OBJECTIVE@#To investigate the expression of EBI3 and p28 mRNA (the 2 subunits of IL-27) in the brain and spinal cord of the model of experimental autoimmune encephalomyelitis (EAE), and to explore their effect on EAE.@*METHODS@#Seventy-two adult female SPF C57BL/6J mice (inbred strain) were randomly divided into a control group, an adjuvant group, and an EAE group. RT-PCR was performed to detect the expression of EBI3 mRNA and p28 mRNA in the brain and spinal cord.@*RESULTS@#The expression of EBI3 mRNA and p28 mRNA was up-regulated at onset in the EAE group, which increased quickly during peak phase and maintained at a high level in the chronic phase. There was significant difference in the expression of EBI3 and p28 mRNA between the EAE group and the control/adjuvant group (P0.05).@*CONCLUSION@#IL-27 may play a role of promoting the morbility of EAE in the early stage, and sustain the inflammatory response in endgame.
Assuntos
Animais , Masculino , Camundongos , Encéfalo , Metabolismo , Doença Crônica , Encefalomielite Autoimune Experimental , Metabolismo , Interleucinas , Genética , Metabolismo , Camundongos Endogâmicos C57BL , Antígenos de Histocompatibilidade Menor , Subunidades Proteicas , Genética , Metabolismo , RNA Mensageiro , Genética , Metabolismo , Receptores de Citocinas , Genética , Metabolismo , Medula Espinal , MetabolismoRESUMO
OBJECTIVE@#To explore the model of chronic experimental autoimmune encephalomyelitis (EAE)for the further study of multiple sclerosis.@*METHODS@#A total of 72 female SPF C57BL/6J mice (inbred strain, aged 8 approximately 10 weeks), were randomly divided into an EAE group, a blank group and an adjuvant group, and each group was divided into 3 subgroups: an onset group, a peak group and a chronic phase group. The EAE group was immunized with mMOG35-55.@*RESULTS@#At the end of the study, and 83.3% of the mice in EAE group suffered the onset, and 8.3% of the mice died. The highest clinical score reached grade 5, namely paralysis of the whole body and then death. In the EAE group, after being immunized first, the mice were all anosis during the first 13 days. They got ill on the third week, and in about 20 approximately 24 days the clinical symptom reached the peak, and in 28 approximately 32 days the chronic phase arrived,when parts of the clinical symptoms got relieved. On the contrary, both the adjuvant group and the blank group were healthy all the time. Characteristic appearance was detected in the EAE group.@*CONCLUSION@#Antigen emulsion, mixture of artificially synthesized mMOG35-55 and complete Freundos adjuvant can successfully induce chronic EAE in the mice. The model of EAE duplicated in our study has the characteristics of high incidence, low death rate and stability, which can be used to carry out further research on multiple sclerosis.