Taipei Medical University Institutional Repository:Item 987654321/44582
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    Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/44582


    Title: Inhibitory effects of ketamine on lipopolysaccharide-induced microglial activation
    Authors: Chang, Yi;Lee, Jie-Jen;Hsieh, Cheng-Ying;Hsiao, George;Chou, Duen-Suey;Sheu, Joen-Rong
    許準榕
    Date: 2009
    Issue Date: 2011-11-14 15:42:52 (UTC+8)
    Abstract: Microglia activated in response to brain injury release neurotoxic factors including nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta). 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 microM) concentration-dependently inhibited lipopolysaccharide (LPS)-induced NO and IL-1beta release in primary cultured microglia. However, ketamine (100 and 250 microM) did not significantly inhibit the LPS-induced TNF-alpha production in microglia, except at the higher concentration (500 microM). 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
    Relation: Mediators of Inflammation.
    Appears in Collections:[醫學科學研究所] 期刊論文

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