Ginsenoside Rb2 inhibits osteoclast differentiation through nuclear factor-kappaB and signal transducer and activator of transcription protein 3 signaling pathway

Biomed Pharmacother. 2017 Aug:92:927-934. doi: 10.1016/j.biopha.2017.05.115. Epub 2017 Jun 8.

Abstract

Ginsenoside-Rb2 (Rb2) is a 20(S)-protopanaxadiol glycoside extracted from ginseng possessing various bioactivities which has drawn considerable interest regarding the area of bone metabolism. However, the effect of Rb2 on osteoclast differentiation remains unknown. In this study, we aimed to investigate the potential role of Rb2 in regulating osteoclast differentiation and the underlying molecular mechanisms. Osteoclast differentiation was induced by receptor activator nuclear factor-kappaB (NF-κB) ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) in mouse RAW 264.7 cells. The results showed that Rb2 dose-dependently inhibited the formation of the tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells and TRAP expression. Furthermore, Rb2 promoted osteoprotegerin expression and bone resorption. The expression of osteoclast marker genes including nuclear factor of activated T cells c1 (NFATc1), c-Fos, OSCAR, and cathepsin K were also markedly inhibited by Rb2 treatment. Moreover, Rb2 significantly inhibited the RANKL-induced NF-κB activation. In addition, Rb2 also markedly suppressed the activation of signal transducer and activator of transcription protein 3 (STAT3) signaling pathway. Interestingly, the knockdown of STAT3 significantly strengthened the inhibitory effect of Rb2 on osteoclast differentiation. Taken together, our study suggests that Rb2 inhibits osteoclast differentiation associated with blocking NF-κB and STAT3 signaling pathways.

Keywords: Ginsenoside-Rb2; NF-κB; Osteoclast differentiation; Osteoporosis; STAT3.

MeSH terms

  • Animals
  • Bone Resorption / genetics
  • Bone Resorption / metabolism
  • Bone Resorption / pathology
  • Cathepsin K / genetics
  • Cathepsin K / metabolism
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation
  • Ginsenosides / pharmacology*
  • Macrophage Colony-Stimulating Factor / pharmacology
  • Mice
  • NF-kappa B / metabolism*
  • NFATC Transcription Factors / genetics
  • NFATC Transcription Factors / metabolism
  • Osteoclasts / drug effects*
  • Osteoclasts / metabolism
  • Osteoclasts / pathology
  • Osteogenesis / drug effects*
  • Osteoprotegerin / metabolism
  • Proto-Oncogene Proteins c-fos / genetics
  • Proto-Oncogene Proteins c-fos / metabolism
  • RANK Ligand / pharmacology
  • RAW 264.7 Cells
  • Receptors, Cell Surface / genetics
  • Receptors, Cell Surface / metabolism
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / drug effects
  • Tartrate-Resistant Acid Phosphatase / metabolism

Substances

  • Ginsenosides
  • NF-kappa B
  • NFATC Transcription Factors
  • Nfatc1 protein, mouse
  • Oscar protein, mouse
  • Osteoprotegerin
  • Proto-Oncogene Proteins c-fos
  • RANK Ligand
  • Receptors, Cell Surface
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Tnfrsf11b protein, mouse
  • ginsenoside Rb2
  • Macrophage Colony-Stimulating Factor
  • Acp5 protein, mouse
  • Tartrate-Resistant Acid Phosphatase
  • Cathepsin K
  • Ctsk protein, mouse