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Inhibitory effects of melatonin on the lipopolysaccharide-induced CC chemokine expression in BV2 murine microglial cells are mediated by suppression of Akt-induced NF-κB and STAT/GAS activity

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Author(s)
권택규
Alternative Author(s)
Kwon, Taeg Kyu
Publication Year
2012
Keyword
AktCC chemokinemelatoninNF-jBSTAT
Abstract
Melatonin influences sleep and circadian rhythm, and it has anti-inflammatory functions. However, the mechanism of its anti-inflammatory roles is not well understood. In our studies, we show that melatonin blocked lipopolysaccharide (LPS)-induced CCL2 (monocyte chemotactic protein-1; MCP-1), CCL5 (Regulated upon Activation, Normal T-cell Expressed, and Secreted), and CCL9 (macrophage inflammatory protein-1γ) chemokine mRNA expression in BV2 murine microglial cells. Melatonin markedly inhibited LPS-induced Akt phosphorylation and NF-κB activation. Furthermore, melatonin inhibited LPS-induced STAT1/3 phosphorylation and interferon-gamma activated sequence (GAS)-driven transcriptional activity. Interestingly, these effects were not associated with reactive oxygen species scavenging effects of melatonin or melatonin receptor signal pathways. Taken together, our results suggested that melatonin has anti-inflammatory functions through down-regulation of chemokine expression by inhibition of NF-κB and STAT/GAS activation in LPS-stimulated BV2 murine microglial cell line.
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Journal of Pineal Research, Vol.52(3) : 296-304, 2012
Type
Article
ISSN
0742-3098
DOI
10.1111/j.1600-079X.2011.00943.x
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34236
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