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Background  Osteoporosis (OP) is a metabolic bone disease due to the imbalance of osteogenesis and bone resorption, in which, bone marrow mesenchymal stem cells (BMSCs) have a significant effect as the seed cells. Recent research has shown the function of  Morusin  on inhibiting osteoclast differentiation in vitro. However, whether  Morusin  can regulate the osteogenic differentiation in addition to the proliferation of BMSCs remains unclear.    Methods  BMSCs were isolated from 4-week-old Wistar rats and then treated with different concentrations of  Morusin  for 3, 5, 7, and 14 days. The proliferation of BMSCs was detected by MTT assay. The effect of  Morusin  on osteogenic differentiation of BMSCs was detected by RT-qPCR, Western blotting, ALP, and Alizarin Red staining. The effect of  Morusin  on Wnt/β-catenin signaling pathway was analyzed by RT-qPCR, Western blotting, and immunofluorescence. Finally, in the ovariectomy-induced osteoporosis model, the anti-osteoporosis activity of  Morusin  was determined by micro-CT, HE, and immunohistochemistry.    Results  The results showed the function of 2.5–10 μM  Morusin  in the promotion of the proliferation in addition to osteogenic differentiation of BMSCs. Moreover, it also has an impact in activating the Wnt/β-catenin signaling pathway via inhibition of β-catenin phosphorylation as well as promotion of its nuclear translocation. Upon Dickkopf-related protein-1 (DKK-1, an inhibitor of the Wnt/β-catenin signaling pathway) was added to the  Morusin ,  Morusin  had a decreased stimulatory osteogenic effect on BMSCs. Finally, in the rat OP model, we found that  Morusin  could also exert anti-osteoporosis activity in vivo.    Conclusions  This study indicates the ability of  Morusin  in the promotion of osteogenic differentiation of BMSCs via the activation of Wnt/β-catenin signaling pathway and also shows the potential of  Morusin  to be an agent for osteoporosis treatment.

stem cell research and therapy

Morusin induces osteogenic differentiation of bone marrow mesenchymal stem cells by canonical Wnt/β-catenin pathway and prevents bone loss in an ovariectomized rat model