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Rubiadin-1-methyl ether from Morinda officinalis How. Inhibits osteoclastogenesis through blocking RANKL-induced NF-κB pathway
- He, Yu-Qiong, Zhang, Qi, Shen, Yi, Han, Ting, Zhang, Quan-Long, Zhang, Jian-Hua, Lin, Bing, Song, Hong-Tao, Hsu, Hsien-Yeh, Qin, Lu-Ping, Xin, Hai-Liang, Zhang, Qiao-Yan
- Biochemical and biophysical research communications 2018 v.506 no.4 pp. 927-931
- IKappaB kinase, Morinda, T-lymphocytes, Western blotting, actin, anthraquinones, bone marrow, bone resorption, cathepsin K, cell viability, gene expression regulation, macrophages, methyl ethers, oncogenes, osteoclasts, phosphorylation, therapeutics, transcription factor NF-kappa B
- Rubiadin-1-methyl ether (RBM) is a natural anthraquinone compound isolated from the root of Morinda officinalis How. In our previous study, RBM was found to have inhibitory effects on the TRAP activity of osteoclasts, which means that RBM may be a candidate for therapy of bone diseases characterized by enhanced bone resorption. However, the further effect of RBM on osteoclasts and the underlying mechanism remain unclear. In the present study, we investigated the effects of RBM isolated from Morinda officinalis How. on osteoclasts derived from bone marrow macrophages (BMMs) and the underlying mechanism in vitro. RBM at the dose that did not affect the viability of cells significantly inhibited RANKL-induced osteoclastogenesis and actin ring formation of osteoclast, while RBM performed a stronger effect at the early stage. In addition, RBM downregulated the expression of osteoclast-related proteins, including nuclear factor of activated T cells cytoplasmic 1 (NFATc1), cellular oncogene Fos (c-Fos), matrix metallopeptidase 9 (MMP-9) and cathepsin K (CtsK) as shown by Western blot. Furthermore, RBM inhibited the phosphorylation of NF-κB p65 and the degradation of IκBα as well as decreased the nuclear translocation of p65. Collectively, the results suggest that RBM inhibit osteoclastic bone resorption through blocking NF-κB pathway and may be a promising agent for the prevention and treatment of bone diseases characterized by excessive bone resorption.