Artemether Inhibits RANKL-Induced Osteoclast Differentiation and Prevents Bone Loss in Ovariectomized Mice

Bone homeostasis is dynamically balanced by osteoclastic bone resorption and osteoblastic bone formation. Increased numbers and enhanced activities of osteoclasts can lead to diseases, such as osteoporosis, aseptic prosthetic loosening, rheumatoid arthritis, and tumor bone metastasis. In postmenopausal women, enhanced osteoclast formation causes excessive bone matrix resorption, less bone mass, and fragile bone mechanical property. Given the importance of osteoclast in osteolytic diseases, inhibiting osteoclast is considered as an effective method for the prevention or treatment of these diseases. In this study, we initially assessed the effects of artemether on osteoclast formation, osteoblast differentiation, and bone mineralization in vitro , further proved by ovariectomy-induced bone loss model in vivo . Here, we found that artemether effectively inhibited osteoclastogenesis in vitro and suppressed ovariectomy-induced bone loss, yet had no effect on osteoblast differentiation and osteoblast-related gene expression. Graphical Abstract