Nacre supplement protects old mice from bone loss

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Background: Glucocorticoid-induced osteoporosis (GIOP) is the most common drug induced osteoporosis, which has a promotion on osteoclasts in the early stage and a long-term inhibition on osteoblasts and osteoclasts.Eldecalcitol, a novel active vitamin D analogue which has been widely studied in the treatment of postmenopausal osteoporosis, but its role in GIOP needs to be further studied.Purpose: This study was aimed to explore the effect and related mechanisms of eldecalcitol on preventing GIOP.Methods: Male C57BL/6 mice were intraperitoneal injected with 10mg/kg/day methylprednisone (MPED) for 4 weeks or 1mg/kg/day dexamethasone (DEX) for 8 weeks to induce GIOP model.At the same time, 50ng/kg/day eldecalcitol was administered orally.Bone quantity and rate of new bone formation were detected by HE staining and calcein/tetracycline labeling.Osteogenic/osteoclastic activity were evaluated using immunochemistry.Further, the MC3T3-E1 cells were treated with DEX and eldecalcitol.The alkaline phosphatase (ALP), alizarin red staining, RT-PCR were used to detect osteoblast differentiation and mineralization.Then, Notch1/Wnt-βcatenin pathway were examined at gene and protein levels.Results: In glucocorticoid (GC) group, the bone mass and rate of bone formation were significantly lower than the control group, accompanied by reduction of osteoblasts and osteoclasts.GC+ eldecalcitol group was characterized by more bone mass and higher rate of bone formation than GC group.Also, eldecalcitol treatment enhanced the activity of osteoblasts and further inhibited osteoclastogenesis when compared with GC group.In vitro, eldecalcitol neutralized the inhibition of osteogenic differentiation and mineralization by DEX in the MC3T3-E1 cells.Further research showed that eldecalcitol activated the Wnt-β-catenin signal and inhibited the Notch signal.Conclusion: Eldecalcitol could prevent the bone loss induced by GC through promoting osteoblast differentiation by Notch1/Wnt-βcatenin signaling.

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