Arctiin abrogates osteoclastogenesis and bone resorption via suppressing RANKL-induced ROS and NFATc1 activation

Related Experiment Video

Updated: Dec 20, 2025

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation
09:37

A RANKL-based Osteoclast Culture Assay of Mouse Bone Marrow to Investigate the Role of mTORC1 in Osteoclast Formation

Published on: March 15, 2018

14.0K

Delong Chen1, Zhen Ye2, Chao Wang3

  • 1Department of Orthopaedic Surgery, Clifford Hospital, Jinan University, Guangzhou 510006, China; School of Biomedical Sciences, University of Western Australia, Perth, Western Australia 6009, Australia.

Pharmacological Research
|May 27, 2020
PubMed

Insights

Arctiin (ARC) from Arctium lappa L. inhibits osteoclast formation and bone loss in osteoporosis models. This compound shows potential as a novel therapeutic agent for treating osteoporosis.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Osteoporosis is a global health challenge due to disrupted bone remodeling.
  • Arctiin (ARC), a component of Arctium lappa L., has shown chemopreventive effects, but its role in bone remodeling is unknown.

Purpose of the Study:

  • To investigate the effect of Arctiin (ARC) on osteoclastogenesis and bone remodeling.
  • To elucidate the underlying molecular mechanisms of ARC's action in bone metabolism.

Main Methods:

  • In vitro studies using receptor activator of nuclear factor-κB ligand (RANKL) to induce osteoclast formation.
  • Analysis of signaling pathways including MAPK, calcium, and NFATc1.
  • In vivo studies using an ovariectomy (OVX) mouse model to assess bone loss.
  • Evaluation of reactive oxygen species (ROS) scavenging enzyme expression via the Nrf2/Keap1/ARE pathway.

Main Results:

  • ARC dose-dependently inhibited RANKL-induced osteoclast formation and bone resorption without cytotoxicity.
  • ARC suppressed RANKL-induced MAPK and calcium signaling pathways.
  • ARC enhanced ROS scavenging enzyme expression and inhibited NFATc1 activation.
  • ARC treatment protected against bone loss in an OVX mouse model.

Conclusions:

  • ARC inhibits osteoclastogenesis by modulating RANKL-induced signaling pathways (MAPK, calcium, NFATc1) and enhancing ROS scavenging via the Nrf2/Keap1/ARE pathway.
  • ARC demonstrates therapeutic potential for preventing ovariectomy-induced bone loss.
  • ARC may serve as a novel therapeutic agent for osteoporosis treatment.
Keywords:
ArctiinBone resorptionOsteoclastRANKL-induced NFATc1 activationROS

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