ArticleBMB reports2023
Ginsenoside Rg2 inhibits osteoclastogenesis by downregulating the NFATc1, c-Fos, and MAPK pathways.
Article in BMB reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Ginsenoside Rg2 fromMolecules (Basel, Switzerland) · 2026Review
- Therapeutic potential of panax ginseng-derived nanovesicles in osteoporosis through enhanced osteoblast.Journal of ginseng research · 2026Article
- Unveiling the Therapeutic Targets and Active Components of Xianlinggubao Capsule in Osteoarthritis and Osteoporosis through Network Pharmacology and Bioinformatic Analysis.Current pharmaceutical design · 2026Article
- Immunomodulatory Activities of Emerging Rare Ginsenosides F1, Rg5, Rk1, Rh1, and Rg2: From Molecular Mechanisms to Therapeutic Applications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Potential ofChinese herbal medicines · 2025Review
- Wnt5a exacerbates pathological bone features and trabecular bone loss in curdlan-injected SKG mice via osteoclast activation.BMB reports · 2025Article
- Exosomes derived from Panax notoginseng promote osteogenic differentiation of rBMSCs via the PI3K/AKT signaling pathway.Frontiers in pharmacology · 2025Article
- Therapeutic Potential of Ginsenosides on Bone Metabolism: A Review of Osteoporosis, Periodontal Disease and Osteoarthritis.International journal of molecular sciences · 2024Review
- Fu-zi decoction attenuate rheumatoid arthritisFrontiers in pharmacology · 2024Article
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Authors and funding
5 authors.
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Abstract
Ginsenosides, among the most active components of ginseng, exhibit several therapeutic effects against cancer, diabetes, and other metabolic diseases. However, the molecular mechanism underlying the anti-osteoporotic activity of ginsenoside Rg2, a major ginsenoside, has not been clearly elucidated. This study aimed to determine the effects of ginsenoside Rg2 on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation. Results indicate that ginsenoside Rg2 inhibits RANKLinduced osteoclast differentiation of bone marrow macrophages (BMMs) without cytotoxicity. Pretreatment with ginsenoside Rg2 significantly reduced the RANKL-induced gene expression of c-fos and nuclear factor of activated T-cells (Nfatc1), as well as osteoclast-specific markers tartrate-resistant acid phosphatase (TRAP, Acp5) and osteoclast-associated receptor (Oscar). Moreover, RANKL-induced phosphorylation of mitogen-activated protein kinases (MAPKs) was decreased by ginsenoside Rg2 in BMM. Therefore, we suggest that ginsenoside Rg2 suppresses RANKLinduced osteoclast differentiation through the regulation of MAPK signaling-mediated osteoclast markers and could be developed as a therapeutic drug for the prevention and treatment of osteoporosis. [BMB Reports 2023; 56(10): 551-556].
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37605614PMC10618073What OpenQuestion holds
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