Effect of cornel iridoid glycoside on microglia activation through suppression of the JAK/STAT signalling pathway
2019-05-15
发表杂志:Journal of Neuroimmunology
发表类型: Research Article
影响因子(IF): 3.478
PMID: 30852182 Pubmed原文链接 全文下载
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.
Based on our findings, CIG might be a promising candidate for the prevention of neurological disorders such as multiple sclerosis (MS).
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.