ArticleJournal of ginseng research2026
Activation of BMPR1b-SMAD pathway by Ginsenoside F1 restores osteoblast function in ovariectomy-induced osteoporosis.
Article in Journal of ginseng research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Osteoblasts are bone-building cells that drive osteogenesis by producing osteoid and promoting its mineralization during development and remodeling. Although ginsenosides from Objectives: This study aimed to elucidate the molecular mechanism by which ginsenoside F1 promotes osteoblast differentiation and evaluate its therapeutic potential in an ovariectomy-induced osteoporosis model. Methods: Bone marrow-derived mesenchymal stem cells and primary osteoblasts were treated with ginsenoside F1. Osteogenic differentiation was analyzed through gene and protein expression of key markers, including Results: Gene and protein expression analyses showed higher levels of osteogenic transcription factors in F1-induced osteoblasts than in untreated cells. RNA-sequencing analysis and molecular docking studies revealed an association between bone morphogenetic protein receptor type 1b (BMPR1b) and SMAD proteins important for mediating osteoblast differentiation following F1 induction. Furthermore, Conclusion: Collectively, these findings suggest that ginsenoside F1 enhances osteoblast differentiation and promotes bone formation under osteoporotic conditions, highlighting its therapeutic potential for bone metabolism disorders.
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