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Dehydromiltirone inhibits osteoclast differentiation in RAW264.7 and bone marrow macrophages by modulating MAPK and

Wei Deng1,2,3, YanBo Huang1,2,3, HaiShang Li1,2,3

  • 1The First Clinical Academy, Guangzhou University of Chinese Medicine, Guangzhou, China.

Frontiers in Pharmacology
|October 10, 2022
PubMed

Insights

Dehydromiltirone (DHT) inhibits osteoclast formation and bone resorption by targeting the MAPK signaling pathway. This study reveals DHT

Area of Science:

  • Pharmacology
  • Biochemistry
  • Cell Biology

Background:

  • Osteoporosis is a metabolic bone disease characterized by decreased bone formation and increased bone resorption.
  • Effective therapeutic agents are crucial for managing osteoporosis and improving patient quality of life.

Purpose of the Study:

  • To investigate the mechanism of Dehydromiltirone (DHT) in treating osteoporosis using network pharmacology and cellular studies.
  • To identify the molecular targets and signaling pathways affected by DHT in the context of osteoporosis.

Main Methods:

  • Network pharmacology analysis including target identification, protein-protein interaction (PPI) analysis, Gene Ontology (GO), and KEGG pathway enrichment.
  • Molecular docking to assess the binding stability of DHT with identified protein targets.
  • In vitro cellular experiments to validate network pharmacology findings and assess DHT's effects on osteoclastogenesis.

Main Results:

  • DHT is implicated in peptide tyrosine phosphorylation, receptor tyrosine kinase, and MAPK signaling pathways.
  • Molecular docking indicated stable binding of DHT to MAPK14, suggesting a role in the MAPK signaling pathway.
  • DHT inhibited osteoclast-associated gene expression (NFATc1, CTSK, c-Fos, Acp5, MMP9) and modulated MAPK and NF-κB signaling pathways.

Conclusions:

  • Dehydromiltirone (DHT) demonstrates anti-osteoclastogenesis activity.
  • DHT inhibits bone resorption by downregulating osteoclast-related gene expression and modulating key signaling pathways.
  • DHT shows potential as a therapeutic agent for osteoporosis.
Keywords:
BMMSMAPKNF-κBdehydromiltironenetwork pharmacologyosteoclastogenesis

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