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-κB activation induced by RANKL. Inhibition may involve interaction of sulforaphane with thiol groups, since it was prevented by reducing agents.

Keywords: Bone Marrow-derived Macrophages, NF-κB, Osteoclastogenesis, RANKL, Sulforaphane, Thiol