ArticleMolecules (Basel, Switzerland)2021
Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway.
Article in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- From depression to bone health: examining the skeletal effects of classical and rapid-acting antidepressants.The international journal of neuropsychopharmacology · 2026Review
- Potential for Drug Repositioning of Midazolam as an Inhibitor of Inflammatory Bone Resorption.International journal of molecular sciences · 2024Article
- Invited Perspective: New Insight into Cadmium-Related Osteoporosis Yields Hope for Prevention and Therapy.Environmental health perspectives · 2024Article
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- 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
- Reactive sulfur and selenium species in the regulation of bone homeostasis.Free radical biology & medicine · 2022Review
- Glucoraphanin Increases Intracellular Hydrogen Sulfide (HNutrients · 2022Article
- Improved repair of rabbit calvarial defects with hydroxyapatite/chitosan/polycaprolactone composite scaffold-engrafted EPCs and BMSCs.Frontiers in bioengineering and biotechnology · 2022Article
- Orcinol Glucoside Improves Senile Osteoporosis through Attenuating Oxidative Stress and Autophagy of Osteoclast via Activating Nrf2/Keap1 and mTOR Signaling Pathway.Oxidative medicine and cellular longevity · 2022Article
- Dietary organosulfur compounds: Emerging players in the regulation of bone homeostasis by plant-derived molecules.Frontiers in endocrinology · 2022Review
- Role of Physical Exercise and Nutraceuticals in Modulating Molecular Pathways of Osteoarthritis.International journal of molecular sciences · 2021Review
- Glucosinolates From Cruciferous Vegetables and Their Potential Role in Chronic Disease: Investigating the Preclinical and Clinical Evidence.Frontiers in pharmacology · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Previous studies have demonstrated that sulforaphane (SFN) is a promising agent against osteoclastic bone destruction. However, the mechanism underlying its anti-osteoclastogenic activity is still unclear. Herein, for the first time, we explored the potential role of autophagy in SFN-mediated anti-osteoclastogenesis in vitro and in vivo. We established an osteoclastogenesis model using receptor activator of nuclear factor kappa-β ligand (RANKL)-induced RAW264.7 cells and bone marrow macrophages (BMMs). Tartrate-resistant acid phosphatase (TRAP) staining showed the formation of osteoclasts. We observed autophagosomes by transmission electron microscopy (TEM). In vitro, we found that SFN inhibited osteoclastogenesis (number of osteoclasts: 22.67 ± 0.88 in the SFN (0) group vs. 20.33 ± 1.45 in the SFN (1 μM) group vs. 13.00 ± 1.00 in the SFN (2.5 μM) group vs. 6.66 ± 1.20 in the SFN (2.5 μM) group), decreased the number of autophagosomes, and suppressed the accumulation of several autophagic proteins in osteoclast precursors. The activation of autophagy by rapamycin (RAP) almost reversed the SFN-elicited anti-osteoclastogenesis (number of osteoclasts: 22.67 ± 0.88 in the control group vs. 13.00 ± 1.00 in the SFN group vs. 17.33 ± 0.33 in the SFN+RAP group). Furthermore, Western blot (WB) analysis revealed that SFN inhibited the phosphorylation of c-Jun N-terminal kinase (JNK). The JNK activator anisomycin significantly promoted autophagy, whereas the inhibitor SP600125 markedly suppressed autophagic activation in pre-osteoclasts. Microcomputed tomography (CT), immunohistochemistry (IHC), and immunofluorescence (IF) were used to analyze the results in vivo. Consistent with the in vitro results, we found that the administration of SFN could decrease the number of osteoclasts and the expression of autophagic light chain 3 (LC3) and protect against lipopolysaccharide (LPS)-induced calvarial erosion. Our findings highlight autophagy as a crucial mechanism of SFN-mediated anti-osteoclastogenesis and show that the JNK signaling pathway participates in this process.
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