Jan 8, 2011

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

Molecular Nutrition & Food Research
Min-Hsiung PanWei-Jen Chen

Abstract

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. 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. MSC might cont...Continue Reading

Mentioned in this Paper

ISYNA1 gene
Phosphorylation Inhibition
Selenomethylselenocysteine, (L)-isomer, 75Se-labeled
Mitogen-Activated Protein Kinases
Mitogen-Activated Protein Kinase 14
Organoselenium Compounds
Murine
Anti-Inflammatory Agents
Protein Phosphorylation
Nitric Oxide Synthase Type II

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