ArticleBMC complementary and alternative medicine2018
Inhibition of RANKL-stimulated osteoclast differentiation by Schisandra chinensis through down-regulation of NFATc1 and c-fos expression.
Article in BMC complementary and alternative medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Wubi Shanyao Pills ameliorate glucocorticoid-induced osteoporosis by regulating bone marrow T cell homing as an immune intermediate to restore bone metabolism.Chinese medicine · 2026Article
- Coptidis Rhizoma Water Extract Attenuates RANKL-Induced Osteoclast Differentiation via MAPK, Akt, and NF-κB Pathways and Prevents Ovariectomy (OVX)-Mediated Bone Loss.International journal of molecular sciences · 2025Article
- The Critical Role of Autophagy in the Pathogenesis of Diabetic Osteoporosis: Mechanisms and Therapeutic Measures.Drug design, development and therapy · 2025Review
- TNF receptor-associated factors: promising targets of natural products for the treatment of osteoporosis.Frontiers in physiology · 2025Review
- Bicyclol Attenuates Obesity-Induced Cardiomyopathy via Inhibiting NF-κB and MAPK Signaling Pathways.Cardiovascular drugs and therapy · 2023Article
- Article
- Dendritic cell-specific transmembrane protein is required for synovitis and bone resorption in inflammatory arthritis.Frontiers in immunology · 2022Article
- Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss.Frontiers in pharmacology · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSchisandra chinenesis (SC) has been reported to have ameliorative effect on osteoporosis. However, the mechanisms underlying the anti-osteoporosis activity of SC have not been clearly elucidated. In the present study, we determined the effects of SC on The receptor activator of NF-kB ligand (RANKL)-induced osteoclastogenesis and its potential mechanism.
methodsRaw 264.7 cells were treated with 0.6, 6 and 60 μg/mL SC in the presence of 100 ng/mL RANKL for 7 days. RANKL-induced osteoclast formation was analyzed by tartrate resistant acid phosphatase (TRAP) staining. The osteoclast differentiation-related factors were confirmed along with TNF-α.
resultsSC inhibits the RANKL-induced osteoclast differentiation in dose-dependent manner within non-toxic concentrations. The supernatant concentrations of TNF-α were significantly decreased by SC treatment. In addition, osteoclastogenesis-related factors, TRAP6 and NF-κB, were markedly decreased by SC in RANKL-induced osteoclasts. Mechanistically, SC reduced the RANKL-triggered NFATc1 and c-fos expressions.
conclusionsTaken together, our data suggest that SC can modulate bone metabolism by suppressing RANKL-induced osteoclast differentiation.
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