• Ginsenoside Rh2 attenuates oxidative stress-induced osteoblast dysfunction by reducing ROS levels, enhancing antioxidant enzyme activity, and improving mitochondrial function.
• Rh2 promotes osteogenic differentiation and mineralization through the nuclear translocation and functional interaction of FoxO1 and β-catenin.
• In an LPS-induced bone loss mouse model, Rh2 administration improves trabecular microstructure, increases osteoblast numbers, and upregulates bone formation serum metabolites.
• The study highlights the FoxO1/β-catenin pathway as a promising therapeutic target for osteoporosis, with Rh2 as a potential clinical or adjuvant therapy.
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