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
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antioxidants*
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Glutathione Peroxidase / genetics*
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Glutathione Peroxidase GPX1
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Gold
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Macrophages
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Metal Nanoparticles / chemistry*
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Mice
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Mice, Inbred C57BL
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Osteoclasts / cytology*
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RANK Ligand / antagonists & inhibitors*
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RANK Ligand / pharmacology
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Reactive Oxygen Species / metabolism
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Receptor Activator of Nuclear Factor-kappa B / antagonists & inhibitors*
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Up-Regulation / genetics
Substances
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Antioxidants
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RANK Ligand
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Reactive Oxygen Species
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Receptor Activator of Nuclear Factor-kappa B
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Gold
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Glutathione Peroxidase
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Glutathione Peroxidase GPX1
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Gpx1 protein, mouse