ArticleDrug design, development and therapy2025
Lobetyolin Suppressed Osteoclastogenesis and Alleviated Bone Loss in Ovariectomy-Induced Osteoporosis via Hindering p50/p65 Nuclear Translocation and Downstream NFATc1/c-Fos Expression.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Mechanisms and therapeutic potential of mitochondrial-targeted therapies in bone repair.Annals of medicine · 2026Review
- Bruceine D suppressed osteoclast formation via STAT3/NF-κB/NFATc1 signaling and protected postmenopausal osteoporosis.Molecular biology reports · 2026Article
- Medicine-food homologous bioactives in metabolic dysregulation-associated osteoporosis: a review of preclinical evidence and potential liver-bone and gut-bone actions.Chinese medicine · 2026Review
- Codonopsis pilosula extract protects against osteoporosis by reducing oxidative stress and inflammation.Journal of molecular histology · 2026Article
- IRG1-itaconate axis in immunometabolism: mechanistic roles and therapeutic potential in inflammatory diseases.Frontiers in immunology · 2026Review
- Dabigatran Attenuates Osteoporosis by Balancing Osteoblastogenesis and Osteoclastogenesis by Targeting PRKAB1 and RELA.Research (Washington, D.C.) · 2026Article
- Targeting Osteoclastogenesis: Sabutoclax reduces tumor-associated osteolysis and tumor burden within the bone microenvironment.American journal of cancer research · 2026Article
- Mechanisms of Microctis Folium in Hyperlipidemia: Integrating Serum Pharmacochemistry, Network Pharmacology, and Transcriptomics.Drug design, development and therapy · 2025Article
- Anti-Inflammatory Modified Fuzi Decoction Antagonizes Synovial TNF-α/TRAF2/NF-κB Signaling to Remedy Osteoarthritis.Drug design, development and therapy · 2025Article
- Lobetyolin ameliorates DSS-induced ulcerative colitis in mice by alleviating inflammation, restoring barrier function, and modulating gut microbiota-metabolite interactions.Frontiers in microbiology · 2025Article
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Authors and funding
10 authors.
Funding
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Abstract
Purpose: To investigate the therapeutic potential of lobetyolin (LBT), a bioactive compound derived from Methods: To investigate the therapeutic potential of LBT in osteoporosis, a multifaceted approach involving network pharmacology and molecular docking was employed to identify relevant targets and elucidate mechanisms of action. In vitro experiments evaluated LBT's impact on osteoclastogenesis, bone resorption, and osteoblast differentiation using bone marrow macrophages (BMMs) and bone marrow mesenchymal stromal cells (BMSCs). The inhibition of RANKL-activated NF-κB signaling and downstream NFATc1/c-Fos pathways was analyzed via Western blot and immunofluorescence. Additionally, an in vivo ovariectomy (OVX)-induced osteoporosis mouse model was utilized to examine the effects of LBT on bone architecture, assessed through micro-CT imaging and histological analyses. Results: LBT effectively suppressed RANKL-driven osteoclast differentiation in vitro without cytotoxic effects, reducing osteoclast numbers, size, and resorptive function. It also downregulated osteoclast-specific genes expressions, inhibited ROS production, and disrupted the NF-κB signaling cascade by blocking p50/p65 nuclear translocation. Moreover, LBT mitigated LPS-induced osteogenic impairment, enhancing osteoblast differentiation and mineralization. In the OVX mouse model, LBT treatment improved bone microstructure. Histological analyses further corroborated LBT's role in reducing osteoclast activity and promoting bone formation. Conclusion: LBT exerts a dual effect on bone remodeling, simultaneously inhibiting osteoclast-mediated bone resorption and promoting osteoblast-driven bone formation. By targeting key pathways such as NF-κB/NFATc1/c-Fos and reducing inflammatory responses, LBT emerges as a potential therapeutic agent for managing PMOP and other conditions associated with excessive bone loss, offering a safer alternative to current treatments.
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