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Protosappanin B activates the Wnt pathway to protect against glucocorticoid-induced osteoblast inhibition and enhance

Jigeng Fan1, Yahui Wang1, Houzhi Yang1

  • 1Tianjin Medical University, Tianjin, China.

Chemico-Biological Interactions
|February 22, 2025
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Summary

Protosappanin B (PB) protects against glucocorticoid-induced osteoporosis by activating Wnt/β-catenin signaling. This natural compound enhances osteoblast function and bone formation, offering potential for preventing bone loss.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoporosis, especially glucocorticoid-induced osteoporosis (GIOP), is a significant health issue linked to poor osteoblast function and bone formation.
  • The Wnt/β-catenin pathway is crucial for bone development and presents a therapeutic target for osteoporosis.
  • Glucocorticoids like dexamethasone (DEX) impair osteoblast activity, contributing to bone loss.

Purpose of the Study:

  • To investigate the potential of Protosappanin B (PB), a natural product, as a Wnt pathway activator for treating glucocorticoid-induced osteoporosis (GIOP).
  • To evaluate PB's protective effects on osteoblast function and bone formation under glucocorticoid exposure.
  • To elucidate the mechanism of action of PB involving the Wnt/β-catenin signaling pathway.

Main Methods:

  • Virtual screening identified PB as a Wnt receptor binder.
  • Osteoblast function was assessed in MC3T3-E1 cells treated with DEX and PB.
  • An in vivo zebrafish model was used to study PB's effects on skeletal development in GIOP.
  • Western blot analysis and Wnt inhibitor (XAV939) treatment were employed to confirm the mechanism.

Main Results:

  • PB promoted osteoblast proliferation, cell cycle progression, and survival, counteracting DEX-induced apoptosis.
  • PB enhanced osteoblast differentiation and mineralization, increasing alkaline phosphatase activity and calcium deposition.
  • In zebrafish, PB ameliorated DEX-induced skeletal defects, improving bone and cartilage formation.
  • PB treatment restored β-catenin levels, activating the Wnt/β-catenin pathway, an effect blocked by XAV939.

Conclusions:

  • Protosappanin B demonstrates protective effects against glucocorticoid-induced osteoblast dysfunction and bone loss.
  • PB acts by activating the Wnt/β-catenin signaling pathway, promoting osteogenesis.
  • PB shows promise as a natural therapeutic agent for preventing GIOP-related bone deterioration.