Bio-Food and Drug Research Center and Department of Biotechnology, College of Biomedical & Health Science, Konkuk University, Chungju 380-701, South Korea.
Nitric Oxide. 2010 Nov 1;23(3):214-9. doi: 10.1016/j.niox.2010.06.005. Epub 2010 Jun 12.
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.
巨噬细胞衍生的一氧化氮（NO）在免疫反应中对抗微生物感染起着重要作用。诱导型一氧化氮合酶（iNOS）产生的过量 NO 与多种疾病和炎症的病理学密切相关。在这项研究中，我们研究了聚乙二醇包覆的金纳米粒子（GNP）对脂多糖（LPS）刺激的 RAW264.7 细胞中 NO 产生的抑制作用及其分子机制。结果发现，GNP 抑制 LPS 诱导的 RAW264.7 细胞中 NO 的产生和 iNOS 的表达。此外，GNP 通过抑制 Akt 活性抑制 LPS 诱导的 NF-κB 激活。GNP 还通过下调干扰素-β（IFN-β）表达来抑制 LPS 诱导的信号转导和转录激活因子 1（STAT1）的磷酸化。我们的结果表明，GNP 通过阻断 LPS 刺激的 RAW264.7 细胞中 NF-κB 和 STAT1 的激活来抑制 NO 的产生和 iNOS 的表达。
