Objective    To explore the effects of prednisolone on the protection of axonal damage in experimental autoimmune encephalomyelitis (EAE)

and the relationship of inflammatory responds with demyelination in the central nervous system.     Methods    Animal model of EAE

also as multiple sclerosis (MS) was established by immunizing C57BL/6J mice with myelin oligodendrocyte glycoprotein peptides

35-55

(MOG

35-55

)

and their clinical signs were scored. Totally 30 immunized C57BL/6J mice were divided into 3 groups

i.e.

untreated group

prednisolone continuously-treated group and prednisolone withdrawal group. Prednisolone at 60 μg/ml was added into the drinking water for the

mice of the later 2 group at the onset of EAE (12-14 d after immunization). The drinking water was continued for the second group till the end of observation (55 d after immunization)

but withdrawn for the mice of the third group at 3 d after the disappearance of symptoms. Axonal damage

inflammation and demyelination were observed by conventional histological method

Bielschowsky staining

and Luxol Fast Blue staining.     Results    Our data indicated that prednisolone could remit the clinical signs of EAE

attenuate axonal damage

eliminate the infiltrate inflammatory cells

and decrease demyelination in central nervous system. In prednisolone withdrawal group

the disease relapsed in 5 to 17 d after the drug stop

and the status of axonal damage was same as that of untreated group.     Conclusion    Prednisolone as a immune regulator can alleviate the signs of EAE and exert transitory protective effect on axonal damage.