Differential suppression of endotoxin-inducible inflammatory cytokines by nuclear factor kappa B (NFκB) inhibitor in rat microglia
Differential suppression of endotoxin-inducible inflammatory cytokines by nuclear factor kappa B (NFκB) inhibitor in rat microglia
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DOI：
10.1016/j.neulet.2006.03.014
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发表时间：
2006-07-03
影响因子：
2.5
通讯作者：
Kurihara, T
中科院分区：
文献类型：
--
作者：
Nakajima, K;Matsushita, Y;Kurihara, T
从信号转导的角度研究了内毒素刺激的小胶质细胞中诱导有害细胞因子白细胞介素1 β（IL-1 β）和肿瘤坏死因子α（TNF α）的分子机制。在未受刺激的大鼠小胶质细胞中不产生细胞因子，但两者都可通过内毒素脂多糖（LPS）刺激显着诱导。用核因子κ B（NF kappa B）抑制剂吡咯烷二硫代氨基甲酸铵（APDC）预处理可显著抑制LPS诱导的IL-1 β，但TNF α则无此作用。APDC实际上被证实抑制I κ B α的降解。和I κ B β，表明NF κ B活化抑制剂的作用。总之，这些结果表明，诱导IL-1 β和TNF α。内毒素刺激的小胶质细胞中，NF κ B B活化水平受到差异调节。(c)2006爱思唯尔爱尔兰有限公司保留所有权利。
The molecular mechanism by which the deleterious cytokines interleukin 1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) are induced in endotoxin-stimulated microglia was investigated from the viewpoint of signal transduction. Neither cytokine is produced in nonstimulated rat microglia, but both are remarkably induced by stimulation with endotoxin lipopolysaccharide (LPS). LPS-inducible IL-1 beta was significantly suppressed by pretreatment with the nuclear factor kappa B (NF kappa B) inhibitor ammonium pyrrolidine dithiocarbamate (APDC), but TNF alpha was not. APDC was actually confirmed to suppress the degradation Of I kappa B alpha. and I kappa B beta in microglia, indicating a role for the inhibitor of NF kappa B activation. Taken together, these results suggest that the induction of IL-1 beta and TNF alpha. in endotoxin-stimulated microglia is differentially regulated at the level of NF kappa B activation. (c) 2006 Elsevier Ireland Ltd. All rights reserved.