Reactive oxygen species mediate Aβ(25-35)-induced activation of BV-2 microglia

被引:59
作者
Kang, JH
Park, EJ
Jou, I
Kim, JH
Joe, EH [1 ]
机构
[1] Ajou Univ, Sch Med, Dept Neurosci, Suwon 442721, South Korea
[2] Ajou Univ, Sch Med, Dept Pharmacol, Suwon 442721, South Korea
[3] Ajou Univ, Sch Med, Brain Dis Res Ctr, Suwon 442721, South Korea
[4] KJIST, Dept Cell Biol, Kwangju 500712, South Korea
关键词
beta-amyloid; microglia; neuroimmunology; reactive oxygen species; signal transduction;
D O I
10.1097/00001756-200105250-00030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Microglial activation induced by beta-amyloid (A beta) is an important cellular response in the pathogenesis of Alzheimer's disease (AD). In this study, we show that reactive oxygen species (ROS) play a role as signaling molecules for the activation of NF-kappaB and induction of IL-1 beta mRNA expression in A beta (25-35)-treated murine microglia BV-2 cells. ROS scavengers such as catalase and superoxide dismutase (SOD) mimetics obviously reduced activation of NF-kappaB and the elevated level of IL-1 beta transcripts induced by A beta (25-35). In addition, the A beta (25-35)-induced NF-kappaB activation and IL-1 beta expression were suppressed by blockers of the ROS generating enzymes such as NADPH oxidase, cyclooxygenase, and lipoxygenase. These data suggest that ROS mediate A beta -induced microglial activation. NeuroReport 12:1449-1452 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:1449 / 1452
页数:4
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