Dihydroartemisinin, an Anti-Malaria Drug, Suppresses Estrogen Deficiency-Induced Osteoporosis, Osteoclast Formation, and RANKL-Induced Signaling Pathways

Lin Zhou, Qian Liu, Mingli Yang, T. Wang, Jun Yao, Jian Wen Cheng, Jinbo Yuan, X. Lin, J. Zhao, Jennifer Tickner, Jiake Xu

    Research output: Contribution to journalArticle

    49 Citations (Scopus)
    301 Downloads (Pure)

    Abstract

    © 2015 American Society for Bone and Mineral Research. Osteoporosis is an osteolytic disease that features enhanced osteoclast formation and bone resorption. Identification of agents that can inhibit osteoclast formation and function is important for the treatment of osteoporosis. Dihydroartemisinin is a natural compound used to treat malaria but its role in osteoporosis is not known. Here, we found that dihydroartemisinin can suppress RANKL-induced osteoclastogenesis and bone resorption in a dose-dependent manner. Dihydroartemisinin inhibited the expression of osteoclast marker genes such as cathepsin K, calcitonin receptor, and tartrate-resistant acid phosphatase (TRAcP). Furthermore, dihydroartemisinin inhibited RANKL-induced NF-?B and NFAT activity. In addition, using an in vivo ovariectomized mouse model, we show that dihydroartemisinin is able to reverse the bone loss caused by ovariectomy. Together, this study shows that dihydroartemisinin attenuates bone loss in ovariectomized mice through inhibiting RANKL-induced osteoclast formation and function. This indicates that dihydroartemisinin, the first physiology or medicine nobel prize discovery of China, is a potential treatment option against osteolytic bone disease.
    Original languageEnglish
    Pages (from-to)964-974
    JournalJournal of Bone and Mineral Research
    Volume31
    Issue number5
    Early online date20 Jan 2016
    DOIs
    Publication statusPublished - May 2016

    Fingerprint Dive into the research topics of 'Dihydroartemisinin, an Anti-Malaria Drug, Suppresses Estrogen Deficiency-Induced Osteoporosis, Osteoclast Formation, and RANKL-Induced Signaling Pathways'. Together they form a unique fingerprint.

  • Cite this