Cumambrin A prevents OVX-induced osteoporosis via the inhibition of osteoclastogenesis, bone resorption, and RANKL signaling pathways

Lin Zhou, Qian Liu, Guoju Hong, Fangming Song, Jinmin Zhao, Jinbo Yuan, Jun Xu, Ren Xiang Tan, Jennifer Tickner, Qiong Gu, Jiake Xu

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3 Citations (Scopus)

Abstract

Being the principal cells responsible for bone resorption and pathologic bone loss, osteoclasts have become the main target for antiresorptive treatment. Cumambrin A is a natural compound isolated from Chrysanthemum indicum L. and belongs to a member of the sesquiterpene lactone family. To date, the therapeutic effect of cumambrin A on osteoporosis and its mechanisms of action are not known. In this study, we found that cumambrin A can significantly inhibit osteoclast formation and bone resorption through the suppression of receptor activator of NF-κB ligand (RANKL)-induced NF-κB and nuclear factor of activated T-cell activity and ERK phosphorylation. Furthermore, cumambrin A inhibits the expression of osteoclast marker genes including cathepsin K, calcitonin receptor, and V-ATPase d2. Using an in vivo ovariectomized mouse model, we showed that cumambrin A protects against estrogen withdrawal-induced bone loss. Collectively, our results reveal that cumambrin A can suppress osteoclast formation, bone resorption, and RANKL-induced signaling pathways, suggesting that cumambrin A is a potential therapeutic agent for the treatment of osteoporosis.-Zhou, L., Liu, Q., Hong, G., Song, F., Zhao, J., Yuan, J., Xu, J., Tan, R. X., Tickner, J., Gu, Q., Xu, J. Cumambrin A prevents OVX-induced osteoporosis via the inhibition of osteoclastogenesis, bone resorption, and RANKL signaling pathways.

Original languageEnglish
Pages (from-to)6726-6735
Number of pages10
JournalFASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volume33
Issue number6
DOIs
Publication statusPublished - 1 Jun 2019

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