Proinflammatory cytokines and apoptosis following glutamate-induced excitotoxicity mediated by p38 MAPK in the hippocampus of neonatal rats

被引：80
作者：
Chaparro-Huerta, V
Rivera-Cervantes, MC
Flores-Soto, ME
Gómez-Pinedo, U
Beas-Zárate, C
机构：
[1] IMSS, CIBO, Div Neurociencias, Mol Neurobiol Lab, Guadalajara, Jalisco, Mexico
[2] Univ Guadalajara, CUCBA, Dept Biol Celular & Mol, Guadalajara 44430, Jalisco, Mexico
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2005年 / 165卷 / 1-2期
关键词：
apoptosis; cytokines; glutamate neuroexcitotoxicity; p38; MAPK; hippocampus;
D O I：
10.1016/j.jneuroim.2005.04.025
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
The proinflammatory cytokines TNF-alpha, IL-1 beta, and IL-6 rise during neuronal damage and activate the apoptotic mitogen-activated protein kinase p38. We studied apoptosis, the levels of TNF-alpha, IL-1 beta, and IL-6, and the cell type producing TNF-alpha in rats at 8, 10, and 14 days of age after neonatal exposure to glutamate, which induces neuronal damage. TNF-alpha production was significantly increased by glutamate, but inhibited by SB203580 (a p38 inhibitor). TNF-alpha, IL-1 beta, and IL-6 mRNA levels increased, but SB203580 did not modify their expression. Thus, the p38 signaling pathway influences the expression of inflammatory genes and its inhibition may offer anti-inflammatory therapy. (C) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码：53 / 62
页数：10
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