Sulforaphane inhibits osteoclastogenesis by inhibiting nuclear factor-kappaB

Mol Cells. 2005 Dec 31;20(3):364-70.

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