ABSTRACT
Platinum nanoparticles (PtNP) exhibit remarkable antioxidant activity. There is growing evidence concerning a positive relationship between oxidative stress and bone loss, suggesting that PtNP could protect against bone loss by modulating oxidative stress. Intragastric administration of PtNP reduced ovariectomy (OVX)-induced bone loss with a decreased level of activity and number of osteoclast (OC) in vivo. PtNP inhibited OC formation by impairing the receptor activator of nuclear factor-kappaB ligand (RANKL) signaling. This impairment was due to a decreased activation of nuclear factor-kappaB and a reduced level of nuclear factor in activated T-cells, cytoplasmic 1 (NFAT2). PtNP lowered RANKL-induced long lasting reactive oxygen species as well as intracellular concentrations of Ca2+ oscillation. Our data clearly highlight the potential of PtNP for the amelioration of bone loss after estrogen deficiency by attenuated OC formation.
Subject(s)
Animals , Mice , Metal Nanoparticles/administration & dosage , Mice, Inbred C57BL , NFATC Transcription Factors/metabolism , Osteoclasts/drug effects , Osteoporosis/drug therapy , Ovariectomy/adverse effects , Oxidative Stress/drug effects , Platinum/administration & dosage , RANK Ligand/genetics , Reactive Oxygen Species/metabolism , Signal TransductionABSTRACT
No abstract available.