Biol Trace Elem Res. 2020 Mar 16. doi: 10.1007/s12011-020-02089-9. [Epub ahead of print]
Aluminum (Al)-induced bone metabolism disorder is a primary cause of osteoporosis. Ginsenoside Rg3 (Rg3) has demonstrated therapeutic properties in the treatment of osteoporosis. The present study aimed to identify potential bone protection mechanisms of Rg3 against Al-induced osteoporosis in rats. In this study, forty healthy male Sprague-Dawley rats were randomly allocated into groups in which they were treated with AlCl3 (64 mg/kg/day) and/or Rg3 (20 mg/kg/day). AlCl3 was given orally to rats for 120 days, and from the 91st day, treated orally with Rg3 for 30 days. Rg3 attenuated AlCl3-induced accumulation of Al by decreasing the bone mineral density in the lumbar spines, femoral metaphysis, and tibia, and inhibited AlCl3-induced oxidative stress in rat bone by decreasing the levels of reactive oxygen species and malondialdehyde, while increasing glutathione peroxidase and superoxide dismutase activity. Rg3 facilitated bone formation by increasing the concentration of calcium, phosphorus, amino-terminal propeptide of type I procollagen, and carboxyl-terminal propeptide of type I procollagen, bone alkaline phosphatase activity in serum, and type I collagen, osteocalcin, and osteopontin protein expressions. Rg3 inhibited bone resorption by decreasing the content of N-terminal cross-linking telopeptide of type I collagen, C-terminal cross-linking telopeptide of type I collagen, and tartrate-resistant acid phosphatase 5b activity in serum. Rg3 promoted the mRNA expression of growth regulation factors by increasing transforming growth factor-β1, bone morphogenetic protein-2, insulin-like growth factor I, and core-binding factor α1. The results demonstrate that Rg3 can significantly attenuate Al accumulation, facilitate bone formation, inhibit bone resorption, resist oxidative stress, and promote the expression of factors that regulate growth. The results indicate that Rg3 is effective in alleviating AlCl3-induced osteoporosis.