摘要

Microglia activated in response to brain injury release neurotoxic factors including nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor- x03B1; (TNF- x03B1;) and interleukin-1 x03B2; (IL-1 x03B2;). Ketamine, an anesthetic induction agent, is generally reserved for use in patients with severe hypotension or respiratory depression. In this study, we found that ketamine (100 and 250x02009; x03BC;M) concentration-dependently inhibited lipopolysaccharide (LPS)-induced NO and IL-1 x03B2; release in primary cultured microglia. However, ketamine (100 and 250x02009; x03BC;M) did not significantly inhibit the LPS-induced TNF- x03B1; production in microglia, except at the higher concentration (500x02009; x03BC;M). Further study of the molecular mechanisms revealed that ketamine markedly inhibited extracellular signal-regulated kinase (ERK1/2) phosphorylation but not c-Jun N-terminal kinase or p38 mitogen-activated protein kinase stimulated by LPS in microglia. These results suggest that microglial inactivation by ketamine is at least partially due to inhibition of ERK1/2 phosphorylation.
原文英語
文章編號705379
期刊Mediators of Inflammation
2009
DOIs
出版狀態已發佈 - 2009

ASJC Scopus subject areas

  • 免疫學
  • 細胞生物學

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