期刊
MOLECULAR NUTRITION & FOOD RESEARCH
卷 59, 期 3, 页码 386-400出版社
WILEY
DOI: 10.1002/mnfr.201400164
关键词
beta-Catenin; Osteoblast; Osteoclast; Rosmarinic acid; Wnt
资金
- Erina Co. Inc.
- MEXT
- Japan Society for the Promotion of Science
- Grants-in-Aid for Scientific Research [26293392, 26293024, 25870188, 26861549] Funding Source: KAKEN
Scope: Bone homeostasis is ensured by the balance between bone formation and resorption. Thus, control of the recruitment, proliferation, and differentiation of bone cells is essential to maintain bone mass. The aim of this study was to elucidate the effects of rosmarinic acid as a potential therapeutic agent on bone metabolism using bone cells and a mouse model. Methods and results: Rosmarinic acid increased alkaline phosphatase activity and induced mineralization in osteoblasts. Addition of rosmarinic acid to cultures of calvarial osteoblastic cells prepared from T-cell factor/beta-catenin TOP-GAL mutant mice strongly induced the expression of LacZ and promoted stabilization of beta-catenin in the cytoplasm of ST2 cells, suggesting that rosmarinic acid affects the canonical Wnt signaling pathway. Moreover, rosmarinic acid inhibited not only osteoclast formation in cocultures of mouse bone marrow cells and osteoblasts, but also receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclastic differentiation in bone marrow-derived macrophages. RANKL-induced p38 mitogen-activated protein kinase and the expression of nuclear factor of activated T cell, c-Jun, and c-Fos were inhibited by rosmarinic acid in bone marrow macrophages. Finally, we confirmed that rosmarinic acid improved bone mass in a soluble RANKL-induced bone loss mouse model. Conclusion: Rosmarinic acid has dual regulatory effects on bone metabolism and may control the bone functions by controlling osteoblastic and osteoclastic differentiation.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据