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We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-κB ligand (RANKL) in osteoclast (OC) precursors. Sulforaphane, an aliphatic isothiocyanate, is a known cancer chemo-preventative agent with antioxidative properties. Nuclear factor-κB (NF-κB) is a critical transcription factor in RANKL-induced osteo-clastogenesis, and electrophoretic mobility shift assays (EMSAs) and assay of NF-κB-mediated secreted alkaline phosphatase (SEAP) revealed that sulforaphane selectively inhibited NF-κB activation induced by RANKL. Inhibition may involve interaction of sul-foraphane with thiol groups, since it was prevented by reducing agents.
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Kang et al. (2005) studied this question.
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