| ObjectiveTo reproduce of MOG35-55 peptide induced EAE animal model, to observe pathological changes of EAE, and to explore the possible pathogenesis of multiple sclerosis (MS).MethodsEach mouse was injected s.c over flanks with MOG35-55, Mycobacterium H37RA , and IFA , injected i.p with pertussis toxin. The pathological changes of EAE were studied with the aid of light and electron microscopy. Consecutive sections were stained with hematoxylin/eosin (HE),Luxol Fast Blue(LFB) , Bielschowsky silver impregnation and TUNEL technique, to assess inflammation, demyelination, axonal pathology and apoptosis respectively.ResultsThe incidence of EAE in immunization animal reached 100%, most mice developed clinical EAE with in 10-16 days of immunization MOG35-55 peptides . Inflammatory cuff around small blood vessels, demyelination around blood vessels and degeneration of neurons were observed under light microscopy. Bielschosky silver impregnation for axons reveals axonal swellings and spheroids. With TUNEL labeling method, the apoptosis of neurons and lymph cell was found. With Electron microscopy, a lot of loose, fused and fragmental spires of myelin sheath were observed. The component of axon is disappeared. In addition, oligodendrocyte progenitor cells have some remyelination in areas of demyelination.ConclusionsThe animal model of EAE induced by MOG35-55 had stable features , a chronic non-remitting course and a high incidence, which w as considered a better model for the study of multiple sclerosis. It is characterized by pervascular inflammation , demyelization, highest incidence of axonal damage, and remyelination in areas of demyelination. The results confirm previous observations of axonal destruction in EAE during demyelization, but not secondary damage in areas of demyelination. It is concluded that MOG35-55 induced EAE may serve as a suitable model for study of axon-protective therapies in inflammatory demyelization conditions. |
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