ArticleBiochemical and biophysical research communications2019
CDDO-Me, Sulforaphane and tBHQ attenuate the RANKL-induced osteoclast differentiation via activating the NRF2-mediated antioxidant response.
Article in Biochemical and biophysical research communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 23 citations in OpenAlex.
- The role of microglia in the development of diabetic retinopathy and its potential clinical application.Human cell · 2025Review
- Ferroptosis and bone metabolic diseases: the dual regulatory role of the Nrf2/HO-1 signaling axis.Frontiers in cell and developmental biology · 2025Review
- Redox Regulation of Immunometabolism in Microglia Underpinning Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2024Review
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- Metallothionein 3 promotes osteoclast differentiation and survival by regulating the intracellular ZnCell death discovery · 2023Article
- NRF2 is essential for iron-overload stimulated osteoclast differentiation through regulation of redox and iron homeostasis.Cell biology and toxicology · 2023Article
- NRF2 and the Moirai: Life and Death Decisions on Cell Fates.Antioxidants & redox signaling · 2023Review
- Article
- High bone mass in mice can be linked to lower osteoclast formation, resorptive capacity, and restricted in vitro sensitivity to inhibition by stable sulforaphane.Cell biochemistry and function · 2022Article
- The Role of NRF2 in Bone Metabolism - Friend or Foe?Frontiers in endocrinology · 2022Review
- Dietary organosulfur compounds: Emerging players in the regulation of bone homeostasis by plant-derived molecules.Frontiers in endocrinology · 2022Review
- Deficiency of optineurin enhances osteoclast differentiation by attenuating the NRF2-mediated antioxidant response.Experimental & molecular medicine · 2021Article
- Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway.Molecules (Basel, Switzerland) · 2021Article
- Cyano Enone-Bearing Triterpenoid Soloxolone Methyl Inhibits Epithelial-Mesenchymal Transition of Human Lung Adenocarcinoma Cells In Vitro and Metastasis of Murine Melanoma In Vivo.Molecules (Basel, Switzerland) · 2020Article
- Osteoclast Multinucleation: Review of Current Literature.International journal of molecular sciences · 2020Review
- The role of natural products in revealing NRF2 function.Natural product reports · 2020Review
- Baitouweng Decoction Ameliorates Ulcerative Colitis in Mice Partially Attributed to Regulating Th17/Treg Balance and Restoring Intestinal Epithelial Barrier.Frontiers in pharmacology · 2020Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Metabolic bone diseases are global public health concerns and are primarily caused by uncontrolled osteoclast (OC) formation and activation. During OC differentiation, intracellular reactive oxygen species (ROS) stimulated by receptor activator of nuclear factor kappa-B ligand (RANKL) can serve as the signaling molecules to promote osteoclastic genes expression. Nuclear factor erythroid-2 related factor 2 (NRF2), a master mediator of cellular antioxidant response, also plays a critical role in OC differentiation through the regulation of redox homeostasis. In this study, we investigated the effects of three NRF2 inducers on osteoclastogenesis, including Bardoxolone methyl (CDDO-Me), Sulforaphane (SFN), and tert-butylhydroquinone (tBHQ). By treating RAW cells with three compounds, we found that NRF2 was activated and its downstream antioxidant genes were upregulated, and the RANKL-induced intracellular ROS production and osteoclastogenesis were impaired. Additionally, the expression of nuclear factor of activated T cells c1 (NFATC1), C-FOS and tumor necrosis factor alpha (TNFα) were inhibited after acute exposures (6 h) to the three compounds. Furthermore, suppressed the expression of osteoclast differentiation-associated genes, tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), matrix metalloproteinase-9 (MMP-9) and dendritic cell-specific transmembrane protein (DC-STAMP) were observed after prolonged exposures (5 days) to the compounds. Taken together, these results suggest that CDDO-Me, SFN and tBHQ attenuate RANKL-induced osteoclastogenesis via activation of NRF2-mediated antioxidant response. Among these compounds, relatively low concentrations of CDDO-Me showed stronger active and inhibitory effects on antioxidant response and osteoclastogenesis, respectively.
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