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NF-kappa B signaling pathway, not IFN-beta/STAT1, is responsible for the selenium suppression of LPS-induced nitric oxide production

Authors
Yun, Cheol-HeuiYang, Jae SeungKang, Seok-SeongYang, YoungCho, Jung HyoSon, Chang GueHan, Seung Hyun
Issue Date
Sep-2007
Publisher
ELSEVIER SCIENCE BV
Keywords
selenium; nitric oxide; toll-like receptor; NF-kappa B; lipopolysaccharide; macrophage
Citation
INTERNATIONAL IMMUNOPHARMACOLOGY, v.7, no.9, pp.1192 - 1198
Journal Title
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume
7
Number
9
Start Page
1192
End Page
1198
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/14638
DOI
10.1016/j.intimp.2007.05.002
ISSN
1567-5769
Abstract
Upon stimulation of macrophages with lipopolysaccharide (LPS), Toll-like receptor 4 recognizes LPS, leading to expression of inducible nitric oxide synthase (iNOS), via MyD88/NF-KB and TRIF/IFN-beta/STAT pathways. Although selenium (Se) was reported to inhibit nitric oxide (NO) production, it is unclear which signaling pathway is inhibited by Se. Here, we investigated how Se inhibits NO production in LPS-stimulated RAW 264.7 cells. When the cells were pretreated with Se for I h followed by LPS treatment, iNOS mRNA expression and subsequent NO production declined significantly in a dose-dependent manner. Se inhibited IKB alpha degradation in the cytosol and NF-KB binding to its recognition site in the nucleus of the LPS-stimulated cells. Meanwhile, Se did not inhibit IFN-beta mRNA induction or STAT1 phosphorylation in the LPS-stimulated cells. These results suggest that Se down-regulates iNOS gene expression and NO production in the LPS-stimulated macrophages through inhibition of the NF-KB activation pathway but not the IFN-beta/STAT1 signaling pathway. (c) 2007 Elsevier B.V. All rights reserved.
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