S-Space College of Medicine/School of Medicine (의과대학/대학원) Pharmacology (약리학전공) Journal Papers (저널논문_약리학전공)
Gold nanoparticles attenuate LPS-induced NO production through the inhibition of NF-kappa B and IFN-beta/STAT1 pathways in RAW264.7 cells
- Ma, Ji Su; Kim, Wan Jae; Kim, Jae Jin; Kim, Tack Joong; Song, Min Dong; Kim, Dong Woo; Lee, Kwang Ho; Moon, Won Kook; Kang, Hyun; Ye, Sang Kyu
- Issue Date
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- NITRIC OXIDE-BIOLOGY AND CHEMISTRY; Vol.23 3; 214-219
- Gold nanoparticles; Interferon-beta (IFN-beta); Inducible nitric synthase (iNOS); Nitric oxide (NO); Signal transducer and activator of transcription 1 (STAT1); Lipopolysaccharide (LPS)
- Macrophage-derived nitric oxide (NO) plays an important role in protection against microbial infection in immune responses. Overproduction of NO by inducible nitric synthase (iNOS) is known to be closely correlated with the pathology of a variety of diseases and inflammations. In this study, we investigated the inhibitory effect of polyethylene glycol coated gold nanoparticles (GNP) on NO production and its molecular mechanism in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. It was found that GNP inhibited LPS-induced NO production and iNOS expression in RAW264.7 cells. Furthermore, GNP suppressed LPS-induced activation of NF-kappa B through the inhibition of Akt activity. GNP also inhibited LPS-induced phosphorylation of signal transducer and activator of transcription 1 (STAT1) via down-regulation of interferon-beta (IFN-beta) expression. Our results suggest that GNP inhibits NO production and iNOS expression through blocking the activation of NF-kappa B and STAT1 in LPS-stimulated RAW264.7 cells. (C) 2010 Elsevier Inc. All rights reserved.
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