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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Intracellular pathways involved in TNF-alpha and superoxide anion release by Abeta(1-42)-stimulated primary human macrophages.
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Intracellular pathways involved in TNF-alpha and superoxide anion release by Abeta(1-42)-stimulated primary human macrophages.

机译:参与TNF-alpha和超氧阴离子释放的Abeta(1-42)刺激的主要人类巨噬细胞的细胞内途径。

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摘要

In this study, the intracellular signal transduction pathways leading to the production of TNF-alpha and superoxide anions by amyloid-beta-stimulated primary human monocyte-derived macrophages was investigated. Using Western blotting and specific inhibitors it is shown that both ERK 1/2 and p38 MAPK signal transduction pathways as well as PKC are involved in the amyloid-beta-stimulated superoxide anion production. In contrast, only ERK 1/2 MAPK seems to be involved in TNF-alpha production: questioning the connection between PKC and ERK 1/2 activation. Our results suggest the use of ERK 1/2 MAPK inhibitors in the prevention of macrophage activation in the context of Alzheimer's disease.
机译:在这项研究中,研究了由淀粉样蛋白-β刺激的人类单核细胞衍生的巨噬细胞导致TNF-α和超氧阴离子产生的细胞内信号转导途径。使用蛋白质印迹和特异性抑制剂,表明ERK 1/2和p38 MAPK信号转导途径以及PKC都参与了由淀粉样β刺激的超氧阴离子的产生。相反,似乎只有ERK 1/2 MAPK参与了TNF-α的产生:质疑PKC和ERK 1/2活化之间的联系。我们的结果表明,在阿尔茨海默氏病的背景下使用ERK 1/2 MAPK抑制剂可预防巨噬细胞活化。

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