These authors contributed equally to this work.
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
Article first published online: 8 JAN 2012
© 2011 John Wiley & Sons A/S
Journal of Pineal Research
Volume 52, Issue 3, pages 296–304, April 2012
How to Cite
Min, K.-J., Jang, J. H. and Kwon, T. K. (2012), 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. Journal of Pineal Research, 52: 296–304. doi: 10.1111/j.1600-079X.2011.00943.x
- Issue published online: 20 MAR 2012
- Article first published online: 8 JAN 2012
- Accepted manuscript online: 5 DEC 2011 03:36AM EST
- Received October 8, 2011; Accepted November 23, 2011.
- CC chemokine;
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.