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

页码：53 / 62

页数：10

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