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Diosmetin inhibits osteoclast formation and differentiation and prevents LPS-induced osteolysis in mice

Siyuan Shao1, Fangsheng Fu1, Ziyi Wang2

  • 1Research Centre for Regenerative Medicine, Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi, China.

Journal of Cellular Physiology
|December 6, 2018
PubMed

Insights

Diosmetin (DIO) effectively inhibits osteoclast formation and bone resorption, offering a potential treatment for osteolytic bone diseases. This natural flavonoid reduces key markers and pathways involved in bone breakdown.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteolytic bone diseases involve excessive osteoclast activity and bone resorption, posing significant clinical challenges.
  • Current treatments focus on inhibiting osteoclasts, but novel therapeutic agents are needed.
  • Diosmetin (DIO), a natural flavonoid, possesses antioxidant and anti-inflammatory properties, but its effect on osteoclast differentiation is largely unknown.

Purpose of the Study:

  • To investigate the effect of Diosmetin (DIO) on osteoclast differentiation and bone resorption.
  • To elucidate the molecular mechanisms underlying DIO's action on osteoclasts.
  • To evaluate the therapeutic potential of DIO in an in vivo model of osteolysis.

Main Methods:

  • Osteoclast differentiation was induced by receptor activator of nuclear factor kappa-B ligand (RANKL) in vitro.
  • Gene expression of osteoclast markers (cathepsin K, NFATc1, Acp5, Ctr, Atp6v0d2, Mmp9) was analyzed.
  • Actin ring formation and bone resorption assays were performed.
  • Western blotting assessed signaling pathways (MAPK) and transcription factors (NFATc1, c-Fos).
  • Reactive oxygen species (ROS) levels were measured.
  • An in vivo mouse model of lipopolysaccharide (LPS)-induced osteolysis was used.

Main Results:

  • DIO dose-dependently inhibited RANKL-induced osteoclast formation.
  • DIO decreased the expression of key osteoclast differentiation markers.
  • DIO attenuated actin ring formation and bone resorption.
  • DIO inhibited the RANKL-induced MAPK signaling pathway and downregulated NFATc1 and c-Fos.
  • DIO reduced RANKL-induced ROS accumulation.
  • DIO significantly ameliorated LPS-induced osteolysis in mice.

Conclusions:

  • Diosmetin (DIO) effectively inhibits osteoclast formation and activation.
  • DIO acts by suppressing the MAPK signaling pathway and reducing ROS production.
  • DIO demonstrates therapeutic potential as a novel agent for treating osteolytic bone diseases.
Keywords:
MAPKdiosmetin (DIO)nuclear factor of activated T-cells 1 (NFATc1)osteoclastsosteolysis

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