Rebaudioside B exerts protective effect against experimental autoimmune encephalomyelitis through inhibition of mitochondrial apoptosis pathway

Background: Multiple sclerosis (MS) is one of the major diseases that threaten human health.This study aimed to evaluate the effect and mechanisms of action of Rebaudioside B (Reb B) in the treatment of MS. Methods: Lipopolysaccharide (LPS) was used to induce an inflammatory response in BV2 microglial cells, which simulates an in vitro MS model.Reb B was screened from small molecular libraries using CCK8 assay and BAX kit. The morphology and functional changes in the LPS- induced BV2 cells were analyzed using the Hoechst 33258 fluorescence staining assay and Western blot (WB).In addition, we established the experimental autoimmune encephalomyelitis (EAE) model of MS in female C57BL/6 mice.We then assessed the clinical symptoms of the EAE mice, and analyzed changes in the expression of key proteins in signal transduction pathways by histopathological staining and WB. Results: Our data showed that the cell viability in the LPS+Reb B group was highest after administration of 10μM Reb B.Compared with the control group, the apoptotic rate, the Bax/Bcl-2 ratio and the expression of cleavage caspase-3 were significantly increased in the BV2 cells under LPS exposure, a finding that contrasted the trend in the Reb B intervention model group. In the EAE model,there was improvement of clinical symptom scores in the drug treatment group.In addition,histological assessment demonstrated that there was less inflammatory infiltration and less demyelination area in the treatment group compared to the model group. Conclusion: Taken together,our data demonstrated that Reb B offers protective effect against EAE microglia through inhibition of an apoptotic pathway.