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Nox2-dependent Neuroinflammation in An EAE Model of Multiple Sclerosis

机译:多发性硬化EAE模型中Nox2依赖性神经炎症

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摘要

BackgroundMultiple sclerosis (MS) is an inflammatory disease of the CNS, characterized by demyelination, focal inflammatory infiltrates and axonal damage. Oxidative stress has been linked to MS pathology. Previous studies have suggested the involvement of NADPH oxidase 2 (Nox2), an enzyme that catalyzes the reduction of oxygen to produce reactive oxygen species, in the MS pathogenesis. The mechanisms of Nox2 activation on MS are unknown. The purpose of this study was to investigate the effect of Nox2 deletion on experimental autoimmune encephalomyelitis (EAE) onset and severity, on astrocyte activation as well as on pro-inflammatory and anti-inflammatory cytokine induction in striatum and motor cortex.
机译:背景多发性硬化症(MS)是中枢神经系统的一种炎症性疾病,其特征在于脱髓鞘,局灶性炎症浸润和轴突损伤。氧化应激已与MS病理相关。先前的研究表明,NADPH氧化酶2(Nox2)是MS发病机理中的一种酶,该酶催化氧的还原以产生活性氧。 MS上Nox2激活的机制尚不清楚。这项研究的目的是调查Nox2缺失对实验性自身免疫性脑脊髓炎(EAE)发作和严重程度,星形胶质细胞活化以及纹状体和运动皮层中促炎和抗炎细胞因子诱导的影响。

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