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Related Experiment Video

Updated: Feb 3, 2026

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
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Helvolic acid attenuates osteoclast formation and function via suppressing RANKL-induced NFATc1 activation.

Kai Chen1, Yu Yuan1,2, Ziyi Wang1

  • 1School of Biomedical Sciences, University of Western Australia, Perth, Western Australia, Australia.

Journal of Cellular Physiology
|October 21, 2018
PubMed
Summary

Helvolic acid effectively inhibits osteoclast formation and bone resorption by suppressing key signaling pathways. This discovery suggests helvolic acid as a potential therapeutic agent for bone lytic disorders like osteoporosis.

Keywords:
helvolic acid (HA)nuclear factor of activated T cells 1 (NFATc1)osteoclastreactive oxygen species (ROS)

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Area of Science:

  • Biochemistry
  • Pharmacology
  • Cell Biology

Background:

  • Osteoclast hyperactivity drives bone lytic disorders, including osteoporosis.
  • Targeting osteoclastogenesis is crucial for treating these bone diseases.
  • Helvolic acid (HA), a mycotoxin, exhibits diverse pharmacological activities.

Purpose of the Study:

  • To investigate the potential of helvolic acid (HA) in inhibiting osteoclast formation and function.
  • To elucidate the molecular mechanisms underlying HA's effects on osteoclastogenesis.
  • To assess HA as a therapeutic candidate for osteoclast-related bone diseases.

Main Methods:

  • In vitro assessment of HA's impact on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and bone resorption.
  • Analysis of NFATc1 activation and expression of its target genes (Ctr, Acp5, Ctsk, Atp6v0d2, Mmp9).
  • Investigation of upstream signaling pathways (ERK, c-Fos, Ca2+ oscillation, NF-κB) and reactive oxygen species generation.

Main Results:

  • HA significantly inhibited RANKL-induced osteoclastogenesis and bone resorption in vitro.
  • HA suppressed nuclear factor of activated T cells 1 (NFATc1) activation and the expression of osteoclastic genes.
  • HA attenuated ERK, c-Fos signaling, Ca2+ oscillation, and reactive oxygen species generation, with minimal effect on NF-κB.

Conclusions:

  • Helvolic acid effectively suppresses osteoclast formation and function by inhibiting key signaling pathways.
  • HA demonstrates potential as a novel therapeutic agent for treating osteoporosis and other osteoclast-related bone diseases.