| ObjectiveWe investigate the expression of Nogo-A and its receptor NgR at the edge of lateral ventricles of rats with experimental autoimmune encephalomyelitis, and explore their function in the happening and development of EAEMethodsThe animal model was established in female Wistar rats by immunizing rats with guinea pig spinal cord homogenate (GPSCH), complete freund's adjuvant (CFA) and pertussis vaccine (PV). Sixty-five Wistar rats were randomly divided into there groups: five rats in normal control group, each thirty rats in EAE group and CFA group, then the later two group were randomly divided into six subgroups, each subgroup have five rats. The animals of control group were sacrificed on the 11th day. The six subgroups of other two groups were sacrificed on the 11th day, the 13th day, the 15th day, the 18th day, the 24th, day and the 30th day. The severity of EAE was scored on a scale 0～5 according to the signs and symptoms. Histological examinations were performed on the sections of brain with the aid of hematoxylin-eosin and Luxol Fast Blue myelin staining. The number of inflammation focus in the central nervous system (CNS) was counted under the optical microscope. The expressions of Nogo-A and NgR in brain tissue were detected by using immunohistochemistry technique. Experimental results were analyzed with SPSS16.0.Results1. The morbility of normal control group and CFA group is 0%, the morbility of EAE group is 86.66%. The clinical symptoms of EAE occurred about 9 days after immunization were induced which lasted 10～12 days. The peak of clinical symptoms took place on the 15th day, meanwhile the histopathology change in the CNS is also most distinct: perivascular cuffing with mononuclear cells, partly neuronal degeneration and demyelination.2. The CNS tissue's hematoxylin-eosin(H-E) staining histopathology results of EAE group's rats indicate that CNS already have inflammation focus on the 11th day, the extent and amount of the inflammation focus increased on the 13th and 15th day, then decreased on the 24th day, reach normal level on the 30th day.3. Immunohistochemistry and analysis results of each group rats indicate that comparing to normal control group and CFA group, the expressions of Nogo-A in brain tissue of EAE were increased on the 11th day (P<0.05), but decreased on the 13th day (P<0.05), re-regulated on 15th day (P<0.05), reach top level on 24th day (P<0.05). the expression level decreased on 30th day, but still higher than CFA group. Comparing with the other subgroups in EAE group, the level of Nogo-A on 24th day was highest. NgR expression level showed no difference compared with normal control group and CFA group on 11th day (p>0.05), the level up-regulated on the 13th, 15th and the 18th day (P<0.05), 24th day subgroup decreased (P>0.05). On 30th day, there was no difference between the three groups (p>0.05). There were also no noticeable differences between the 13th, 15th and 18th subgroup of EAE group.4. The expression of NgR was positively correlated with inflammation focus and the correlation coefficients was 0.437, so was with neurological deficit scores, correlation coefficients was 0.43.Conclusion1. Nogo-A interact with NgR may be involved in the axonal damage in the early stage and inhibition of axonal regeneration in the late period of EAE.2. That NgR increase in the middle stage of EAE may be associated with the adhesion, migration, and activation of inflammatory cells. There may be other receptors of Nogo-A mediate the axonal inhibition in the late stage of EAE.
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