期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 592, 期 1-3, 页码 55-61出版社
ELSEVIER
DOI: 10.1016/j.ejphar.2008.06.099
关键词
SB239063; inflammation; neuroprotection; neurogenesis; microglia; ischemia
资金
- Saxony-Anhalt [3594M/0405M]
We investigated the effect of the p38 mitogen-activated protein kinase inhibitor SB239063 on inflammation and neurogenesis after ischemia in organotypic hippocampal slice cultures. Our study shows that after oxygen-glucose deprivation, the p38 mitogen-activated protein kinase (MAPK) and the extracellular-signal-regulated kinase 112 (ERK1/2) are strongly activated. The p38 MAPK phosphorylation returned to basal levels within 1 h after oxygen-glucose deprivation, whereas the ERK1/2 phosphorylation reached the basal level only after 24 h. Treatment with 20 mu M and 100 mu M SB239063 strikingly reduced cell death after oxygen-glucose deprivation and significantly diminished microglia activation in the cornu ammonis (CA-region), but not in the area dentata. Levels of the pro-inflammatory cytokine IL-1 beta were reduced by 84% after treatment with SB239063 whereas the cytokines IL-6 and TNF-alpha were not affected. After 6 days, neurogenesis was significantly increased in the posterior periventricle. Based on these findings, our study shows that anti-inflammatory treatment with SB239063 reduces cell death, inflammation and microglia activation and, at high concentrations, enhances the oxygen-glucose deprivation-induced neurogenesis in the posterior periventricle. (C) 2008 Elsevier B.V. All rights reserved.
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