Abstract
INTRODUCTION: Multiple sclerosis is a chronic autoimmune demyelinating disorder predominantly affecting the white matter of the central nervous system, with experimental autoimmune encephalomyelitis (EAE) serving as its classical animal model. Irisin, a glycosylated protein derived from the proteolytic cleavage of fibronectin type III domain-containing protein 5, plays a significant role in metabolic regulation and inflammatory modulation within the organism. METHODS: In this study, we systematically investigated the therapeutic effects and underlying mechanism of Irisin on EAE and BV2 microglial cells through comprehensive methodologies including quantitative real-time polymerase chain reaction, immunofluorescence staining and western blot. RESULTS: Irisin exerts neuroprotective effects in EAE mice, significantly ameliorating both clinical and pathological manifestations of the disease. Mechanistically, Irisin attenuated inflammatory response and reduced the number of microglia through NF-κBp65 signaling pathway. CONCLUSION: In conclusion, these results collectively suggest that Irisin alleviates EAE progression by suppressing microglia activation via the NF-κBp65 pathway, highlighting its potential as a promising therapeutic target for multiple sclerosis treatment.