Gold nanoparticles attenuate LPS-induced NO production through the inhibition of NF-kappaB and IFN-beta/STAT1 pathways in RAW264.7 cells.

Abstract

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-kappaB 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-kappaB and STAT1 in LPS-stimulated RAW264.7 cells.

• Authors: Ji Su Ma, Wan Jae Kim, Jae Jin Kim, Tack Joong Kim, Sang Kyu Ye, Min Dong Song, Hyun Kang, Dong Woo Kim, Won Kook Moon, Kwang Ho Lee
• Journal: Nitric oxide : biology and chemistry (Nitric Oxide) Vol. 23 Issue 3 Pg. 214-9 (Nov 01 2010) ISSN: 1089-8611 [Electronic] United States
• PMID: 20547236 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright 2010 Elsevier Inc. All rights reserved.

Chemical References

• Lipopolysaccharides
• NF-kappa B
• RNA, Messenger
• STAT1 Transcription Factor
• Nitric Oxide
• Polyethylene Glycols
• Gold
• Interferon-beta
• Nitric Oxide Synthase Type II

Topics

• Animals
• Cell Survival (drug effects)
• Cells, Cultured
• Gold (chemistry, pharmacology)
• Interferon-beta (antagonists & inhibitors, metabolism)
• Lipopolysaccharides (antagonists & inhibitors, pharmacology)
• Metal Nanoparticles (chemistry)
• Mice
• NF-kappa B (antagonists & inhibitors, metabolism)
• Nitric Oxide (biosynthesis)
• Nitric Oxide Synthase Type II (genetics, metabolism)
• Polyethylene Glycols (chemistry, pharmacology)
• RNA, Messenger (drug effects, genetics)
• Reverse Transcriptase Polymerase Chain Reaction
• STAT1 Transcription Factor (antagonists & inhibitors, metabolism)