Objective To study the protective effect and related mechanisms of rebaudioside B in the experimental autoimmune encephalomyelitis(EAE)model.Methods BV2 cells were cultured and randomly divided into normal control group,lipopolysaccharide(LPS)inflammatory cell model group,and rebaudioside B intervention group.The LPS inflammatory cell model was prepared by incubating BV2 cells with 1 μg/mL LPS for 24 hours.The rebaudioside B intervention group was given 10 μmol/L rebaudioside B for 4 hours before modeling.Flow cytometry was used to detect cell cycle and apoptosis,immunofluorescence was used to observe cell morphology,and western blot was used to detect the expression of Caspase-3,Bax,and Bcl-2 in cells.Thirty female C57BL/6 mice of 6-8 weeks of age were selected and randomly divided into a normal control group,EAE model group,and rebaudioside B intervention group,with 10 mice in each group.The EAE animal model was constructed by subcutaneous injection of MOG35-55 peptide.On the 8th day after the modeling,mice in the rebaudioside B intervention group were injected intraperitoneally with rebaudioside B(1 mg/kg)for 15 d.HE staining was used to observe the histopathological changes in the spinal cord of mice,western blot was used to detect the expression of Caspase-3,Bax,and Bcl-2 in the spinal cord,and the apoptotic bodies in the brain of mice were observed by transmission electron microscopy.Results(1)The results of cellular experiments:compared with the normal control group,the LPS inflammatory cell model group showed a decreased proportion of cells in the S phase,significant nuclear chromatin condensation,increased apoptosis rate,increased expression level of Caspase-3,and elevated Bax/Bcl-2 ratio(all P<0.01).Compared with the LPS inflammatory cell model group,the proportion of cells in the S phase was up-regulated in the rebaudioside B intervention group,and chromatin condensation in the nucleus was improved.The apoptosis rate,the expression level of Caspase-3,and the Bax/Bcl-2 ratio was decreased(all P<0.01).(2)Results of animal experiments:compared with the normal control group,mice in the EAE model group showed increased inflammatory cell infiltration in the spinal cord tissue,increased expression level of Caspase-3 and elevated Bax/Bcl-2 ratio(all P<0.01),and abnormal cell morphology in the brain tissue,with the appearance of apoptotic vesicles.Compared with the EVE model group,the spinal cord tissue of mice rebaudioside B intervention group showed a decrease in the expression level of Caspase-3,a decrease in the Bax/Bcl2 ratio(all P<0.01),and normal cell morphology of the mouse brain tissue.Conclusions Rebaudioside B has neuroprotective effect in EAE model mice,and its mechanism is related to the inhibition of apoptosis pathway by rebaudioside B.