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Mediators of InflammationVolume 2009 2009, Article ID 705379, 7 pages

Research Article

Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, School of Medicine, Fu-Jen Catholic University, 24205 Taipei, Taiwan

Department of Pharmacology, Taipei Medical University, 11031 Taipei, Taiwan

Department of Surgery, Mackay Memorial Hospital, Taipei 10449, Taiwan

Received 5 September 2008; Accepted 24 January 2009

Academic Editor: Vera L. Petricevich

Copyright © 2009 Yi Chang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Microglia activated in response to brain injury release neurotoxic factors including nitric oxide NO and proinflammatory cytokines such as tumor necrosis factor- TNF- and interleukin-1 IL-1 . 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 250  concentration-dependently inhibited lipopolysaccharide LPS-induced NO and IL-1 release in primary cultured microglia. However, ketamine 100 and 250  did not significantly inhibit the LPS-induced TNF- production in microglia, except at the higher concentration 500  . 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.

Autor: Yi Chang, Jie-Jen Lee, Cheng-Ying Hsieh, George Hsiao, Duen-Suey Chou, and Joen-Rong Sheu



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