Abstract
We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-kB ligand (RANKL) in osteoclast (OC) precursors. Sulforaphane, an aliphatic isothiocyanate, is a known cancer chemo-preventative agent with anti-oxidative properties. Nuclear factor-kB (NF-kB) is a critical transcription factor in RANKL-induced osteoclastogenesis, and electrophoretic mobility shift assays (EMSAs) and assay of NF-kB-mediated secreted alkaline phosphatase (SEAP) revealed that sulforaphane selectively inhibited NF-kappaB activation induced by RANKL. Inhibition may involve interaction of sulforaphane with thiol groups, since it was prevented by reducing agents.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Alkaline Phosphatase / metabolism
-
Animals
-
Bone Marrow Cells / drug effects
-
Bone Marrow Cells / metabolism
-
Carrier Proteins / pharmacology
-
Cells, Cultured
-
Electrophoretic Mobility Shift Assay
-
Isothiocyanates
-
Membrane Glycoproteins / pharmacology
-
Mice
-
Mice, Inbred C57BL
-
NF-kappa B / antagonists & inhibitors*
-
Osteoclasts / drug effects*
-
Osteoclasts / metabolism
-
RANK Ligand
-
Receptor Activator of Nuclear Factor-kappa B
-
Sulfhydryl Compounds / metabolism
-
Thiocyanates / pharmacology*
Substances
-
Carrier Proteins
-
Isothiocyanates
-
Membrane Glycoproteins
-
NF-kappa B
-
RANK Ligand
-
Receptor Activator of Nuclear Factor-kappa B
-
Sulfhydryl Compounds
-
Thiocyanates
-
Tnfrsf11a protein, mouse
-
Tnfsf11 protein, mouse
-
Alkaline Phosphatase
-
sulforafan