Abstract
Osteoclasts are the only cells that can resorb bone and they are produced from monocytes/macrophages in the presence of M-CSF and RANKL and are activated in vivo by an immune response. Usnic acid is a secondary metabolite of lichen and has a unique dibenzofuran skeleton. It has been used for years in cosmetics, fragrances, and traditional medicines. It has a wide range of bioactivities, including anti-inflammatory, anti-bacterial, anti-cancer, anti-viral, and so on. However, the anti-osteoclastogenic activity of usnic acid has not been reported yet. In this study, we investigated whether usnic acid could affect RANKL-mediated osteoclastogenesis. Usnic acid significantly inhibited RANKL-mediated osteoclast formation and function by reducing the transcriptional and translational expression of NFATc1, a master regulator of osteoclastogenesis. In addition, it prevented lipopolysaccharides (LPS)-induced bone erosion in mice. Taken together, our results suggest that usnic acid might be a potential candidate for the treatment of osteoporosis.