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山茱萸环烯醚萜苷通过抑制 JAK/STAT 信号通路对小胶质细胞活化的影响。

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

机构信息

Xuan Wu Hospital of Capital Medical University, 45 Changchun Street, Beijing 100053, PR China; Institute of Clinical Pharmacology, Guangzhou University of Chinese Medicine, 12 Jichang Road, Guangzhou, Guangdong Province 510405, PR China.

Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; China National Clinical Research Center for Neurological Diseases, China.

出版信息

J Neuroimmunol. 2019 May 15;330:96-107. doi: 10.1016/j.jneuroim.2019.01.014. Epub 2019 Mar 4.

DOI:10.1016/j.jneuroim.2019.01.014
PMID:30852182
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 MOG 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).

摘要

迄今为止,山茱萸环烯醚萜苷(CIG)的作用(CIG 是从山茱萸中提取的主要成分),对小胶质细胞激活的影响还没有被阐明。我们通过用 MOG 肽皮下免疫诱导实验性自身免疫性脑脊髓炎(EAE)模型,建立了多发性硬化症(MS)的小鼠模型,这会导致神经炎症和小胶质细胞激活。我们的数据表明,CIG 延迟了 EAE 的发作,改善了症状的严重程度,并抑制了不同脑区小胶质细胞的激活。此外,我们还发现 CIG 通过减少促炎细胞因子、趋化因子的表达和释放,以及抑制 JAK/STAT 细胞信号通路中的磷酸化,具有调节小胶质细胞极化的治疗潜力。基于我们的发现,CIG 可能是预防多发性硬化症(MS)等神经紊乱的有前途的候选药物。

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