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Ginsenosides Rg3 attenuates glucocorticoid-induced osteoporosis through regulating BMP-2/BMPR1A/Runx2 signaling
Xiaonan Zhang1, Kang Chen1, Bo Wei1
1Department of Sports Medicine and Joint Surgery, The First Affiliated Hospital of China Medical University, Shenyang 110001, People's Republic of China.
Abstract:
Glucocorticoid-induced osteoporosis (GIOP) is the primary cause of secondary osteoporosis and the existing therapeutic strategies are limited. The aim of this study is to evaluate the effects of ginsenosides (GS) Rg3 on dexamethasone (DEX)-induced osteoporosis in vivo and in vitro. GIOP rat was established by DEX injection for 5 weeks and treated by GS Rg3 10 or 20 mg/kg. Body weight and bone mineral density (BMD) of rats were measured at the beginning and the end of the experiment. Histological changes of femurs were observed using HE staining. The in vitro model was established on primary osteoblasts induced by DEX. CCK-8 assay was used to test the cell viability. Bone metabolism markers in serum or primary osteoblasts were detected using biochemical kits. Real time PCR and western blot were used to measure nuclear factor-kappa B ligand (RANKL), osteoprotegerin (OPG), bone morphogenic protein-2 (BMP-2), BMP receptor 1A (BMPR1A) and Runx2 expression. The results demonstrated that GS Rg3 prevented DEX-induced body weight and BMD reduction, enhanced secretion of bone formation markers and decreased bone resorption markers. In addition, GS Rg3 was found to prevent the suppression of BMP-2/BMPR1A/Runx2 signals induced by DEX both in GIOP rats and primary osteoblasts. Inhibition of BMP-2 by noggin completely blocked the bone-alkaline phosphatase-secretion-promoted effect of GS Rg3 in vitro. These data suggest that GS Rg3 attenuates GIOP through regulating BMP-2 signaling pathway. This study provides a potential drug candidate for GIOP therapy.
Insights
Ginsenoside Rg3 (GS Rg3) effectively combats glucocorticoid-induced osteoporosis (GIOP) by preserving bone mineral density and regulating bone metabolism. This natural compound shows promise as a therapeutic agent for GIOP.
Area of Science:
- Pharmacology
- Osteoporosis Research
- Natural Product Chemistry
Background:
- Glucocorticoid-induced osteoporosis (GIOP) is a significant clinical challenge with limited treatment options.
- Existing therapies for GIOP have limitations, necessitating the exploration of novel therapeutic agents.
Purpose of the Study:
- To investigate the therapeutic potential of ginsenoside Rg3 (GS Rg3) in mitigating dexamethasone (DEX)-induced osteoporosis.
- To elucidate the underlying molecular mechanisms of GS Rg3 action in both in vivo and in vitro models of GIOP.
Main Methods:
- Established a GIOP rat model using dexamethasone (DEX) and treated with varying doses of GS Rg3.
- Assessed body weight, bone mineral density (BMD), and femur histology in vivo.
- Utilized primary osteoblasts for in vitro studies, evaluating cell viability, bone metabolism markers, and gene/protein expression (RANKL, OPG, BMP-2, BMPR1A, Runx2) via PCR and Western blot.
Main Results:
- GS Rg3 treatment prevented DEX-induced reductions in body weight and BMD in rats.
- GS Rg3 administration modulated bone metabolism markers, increasing bone formation and decreasing bone resorption.
- GS Rg3 preserved the BMP-2/BMPR1A/Runx2 signaling pathway, crucial for osteoblast differentiation, which was suppressed by DEX.
Conclusions:
- Ginsenoside Rg3 demonstrates significant efficacy in attenuating glucocorticoid-induced osteoporosis.
- The therapeutic effects of GS Rg3 are mediated through the regulation of the BMP-2 signaling pathway.
- GS Rg3 represents a promising candidate for the development of novel therapeutic strategies for GIOP.
