| Objective: To investigate the effects of EAE rat in terms of neurological inflammatory pathways by appling carbachol to intervene EAE rats, detectting the expression changes of astrocyte marker GFAP and pathological changes.Methods:Making EAE rat models, Normal group was not modeling. Intervening with Carbachol through ventricle in experimental group, saline in control group and normal group. After intervention, rats were observed incidence, recorded neurological score. Upon termination of observation, remove the rat brain and spinal cord, to make of sliced, observe inflammatory infiltration by HE staining, calculate the average optical density of GFAP with Image-proplus software by immunohistochemistry. Finally, statistic the differences between each set of observed indicators.Results:Onset latency was not statistically significant between Carbachol intervention group and general intervention group(P> 0.05).The neurological deficit score of peak incidence between the two groups was not statistically significant (P>0.05).9 of carbachol intervention group rats in pathogenesis and 11 of the general group in the end of the experiment. There was no significant difference in the morbidity (P> 0.05). There was no significant difference in body weight of rats. HE staining: carbachol intervention group EAE inflammatory cell infiltration was significantly lower than general intervention EAE group. Immunohistochemical staining: the difference of GFAP expression in cerebral, spinal cord was statistically significant between carbachol intervention group and ordinary intervention group (P<0.05).Conclusion: Carbachol intervention may inhibit the activation and proliferation of astrocytes in early EAE rats. Meanwhile carbachol intervention can significantly reduce the infiltration of inflammatory cells.The study results show that the neural anti-inflammatory pathway may provide new ideas for EAE/MS treatment. |
PDF Full Text Request