A previous study revealed that rutin is the main component of Eucommia flavonoids that exerts a protective effect against osteopenia. The bone density and trabecular bone number of osteoporosis model rats can be significantly improved after treatment with rutin. Further study using whole gene expression profiling revealed that FNDC1, a fibronectin type III domain-containing protein, may be a novel bone metabolism-related factor that is decreased in rutin-treated rats. The mechanism underlying the effects of rutin treatment on osteoporosis is important to explore. Micro-CT, western blotting, quantitative PCR, transmission electron microscopy, and Alizarin Red mineralization staining assays were performed to evaluate bone density, FNDC1 expression and autophagy to determine whether FNDC1 might play a significant role in rutin-inhibited trabecular bone loss in rats. FNDC1 expression was high in the osteoporosis group, whereas rutin treatment facilitated FNDC1 downregulation. In addition, rutin promoted bone marrow mesenchymal stem cell autophagy by inhibiting phosphorylated Akt in osteoporosis. In summary, our study shows that rutin could regulate FNCD1 level and autophagy through the Akt/mTOR signaling pathway to provide a novel therapeutic strategy for osteoporosis.
Keywords: FNDC1; Rutin; autophagy; postmenopausal osteoporosis.
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