Effect of cornel iridoid glycoside on microglia activation through suppression of the JAK/STAT signalling pathway

Abstract

The effect of cornel iridoid glycoside (CIG), main component extracted from Cornus officinalis, on microglia activation has not been elucidated so far. We induced a mouse model of multiple sclerosis (MS), namely, the experimental autoimmune encephalomyelitis (EAE) model by immunization subcutaneously with the MOG35–55 peptide, which causes neuroinflammation and microglia activation. Our data demonstrated that CIG delayed the onset of the EAE, ameliorated the severity of the symptoms and inhibited the activation of microglia in different brain regions. In addition, we also found that CIG has therapeutic potential by modulating microglia polarization by reducing the expression and release of proinflammatory cytokines, chemokines and inhibiting phosphorylation in the JAK/STAT cell signalling pathway. Based on our findings, CIG might be a promising candidate for the prevention of neurological disorders such as multiple sclerosis (MS).