Gold nanoparticles inhibited the receptor activator of nuclear factor-κb ligand (RANKL)-induced osteoclast formation by acting as an antioxidant

Biosci Biotechnol Biochem. 2010;74(11):2209-13. doi: 10.1271/bbb.100375. Epub 2010 Nov 7.

Abstract

Gold nanoparticles inhibited osteoclast (OC) formation induced by the receptor activator of nuclear factor-κB ligand (RANKL) in bone marrow-derived macrophages (BMMs). This was accompanied by a decreased level of tartrate-resistant alkaline phosphatase (TRAP) and less activation of nuclear factor (NF)-κB. The nanoparticles also reduced the production of reactive oxygen species (ROS) in response to RANKL and upregulated RANKL-induced glutathione peroxidase-1 (Gpx-1), suggesting a role as an antioxidant in the BMM. The inhibitory effects on OC formation might have been due to elevated defense against oxidative stress.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants*
  • Glutathione Peroxidase / genetics*
  • Glutathione Peroxidase GPX1
  • Gold
  • Macrophages
  • Metal Nanoparticles / chemistry*
  • Mice
  • Mice, Inbred C57BL
  • Osteoclasts / cytology*
  • RANK Ligand / antagonists & inhibitors*
  • RANK Ligand / pharmacology
  • Reactive Oxygen Species / metabolism
  • Receptor Activator of Nuclear Factor-kappa B / antagonists & inhibitors*
  • Up-Regulation / genetics

Substances

  • Antioxidants
  • RANK Ligand
  • Reactive Oxygen Species
  • Receptor Activator of Nuclear Factor-kappa B
  • Gold
  • Glutathione Peroxidase
  • Glutathione Peroxidase GPX1
  • Gpx1 protein, mouse