To Establish Mice Model Of Experimental Optic Neuritis

Objective To establish mice model of autoimmune optic neuritis induced by the petide myelin oligodendrocyte glycoprotein(MOG35-55).Methods C57BL/6 mice were induced to optic neuritis which were injected by MOG35-55 peptide. At days 0,7,14,20,30,40 post immunization, visual evoked potential (f-VEP) and flash electroretinogram (F-ERG), Optical Coherence Tomography (OCT) test performed in experimental group and control group to observe the changes of visual function in mice; at the same time, at days 0,14,20,30,40 post immunization, optic nerve were stained with hymatoxylin/eosin, Luxol Fast Blue staining and TUNEL to assess inflammation, demyelination axonal pathology, and measuring Apoptosis of RGCs. electron microscope observe mice tissue pathological changes.Results (1) the thickness of RNFL in OCT:EAE group is thinner (P< 0.05 CON vs group). (2) f-VEP:the latency of EAE group is prolonged and the amplitude of EAE group is decreased (vs< 0.05 CON P group); the 40 day is recovered. (3) f-ERG:the latency of EAE wave in group B was prolonged (except for 40 days), but the latency of B was decreased(P< 0.05 CON vs group). (4) HE staining:optic nerve of EAE group has same or a large number of inflammatory cell (the most is days of 20,30), the retina of the nerve fiber layer has varying degrees of edema. (5) LFB staining:EAE group appear the myelin sheath depigmentation with the time going, which the 30 days is most obvious, At days 40, demyelination appeared regeneration. (6) electron microscopy:EAE group appear myelin edema, demyelination, myelin sheath with the time going, At days of 40 begin to reconstruction. (7) TUNEL:with the course of disease, more and more apoptotic cells appear on the EAE group (vs< 0.05 CON P group).Conclusions The animal model of EAE induced by MOG35-55 had stable features. It is concluded that MOG35-55 induced EAE may serve as a suitable model for study of neuritis-protective therapies in inflammatory demyelization conditions.