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Se-methylselenocysteine inhibits lipopolysaccharide-induced NF-κB activation and iNOS induction in RAW 264.7 murine macrophages

✍ Scribed by Min-Hsiung Pan; Huei-Mei Hong; Chih-Li Lin; Ai-Zhi Jhang; Jie-Heng Tsai; Vladimir Badmaev; Kalyanam Nagabhushanam; Chi-Tang Ho; Wei-Jen Chen

Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
297 KB
Volume
55
Category
Article
ISSN
1613-4125

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✦ Synopsis

Abstract

Scope: Se‐methyl‐L‐selenocysteine (MSC), a naturally occurring organoselenium compound, has shown cancer chemopreventive activity against several types of cancer. Herein, the effect of MSC on the inflammatory response in lipopolysaccharide (LPS)‐activated murine RAW 264.7 macrophage cells was investigated.

Methods and results: The present results demonstrated that MSC markedly inhibited LPS‐induced production of NO in a dose‐dependent pattern with decreased mRNA and protein levels of inducible nitric oxide synthase (iNOS). MSC also reduced nuclear translocation of p65 and p50 subunits of nuclear factor‐κB (NF‐κB), a critical transcription factor necessary for iNOS expression, accompanied with downregulation of LPS‐triggered NF‐κB‐dependent gene expression evaluating by a luciferase reporter. Inhibition of nuclear translocation by MSC might result from the prevention of the inhibitor of NF‐κB from phosphorylation and consequent degradation via suppression inhibition of phosphorylation of IκB kinase α/β. Exploring the action mechanism involved, MSC can reduce the phosphorylation/activation of mitogen‐activated protein kinases (MAPKs) related to NF‐κB activation induced by LPS, including p38 MAPK and c‐Jun N‐terminal kinase in RAW 264.7 cells.

Conclusion: MSC might contribute to the potent anti‐inflammatory effect in LPS‐activated RAW 264.7 cells via downregulation of NF‐κB activation and iNOS expression, suggesting that MSC may be considered as a therapeutic candidate for chronic inflammatory diseases.

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