Forsythoside A Inhibits Osteoclast Genesis and Bone Resorption via Suppressing NF-kappa B Signaling

Over-activation of osteoclastogenesis is involved in osteoporosis and inflammatory osteolysis. Limited drugs are used up to now to treat these diseases with minor complications. It is of great importance to explore the mechanism behind these diseases and seek novel target to take control of the disorganized osteoclastogenesis. In our study, we firstly found that forsythoside A (FT-A) inhibited LPS-induced calvaria osteolysis via suppressing the formation or recruitment of osteoclasts. FT-A inhibited osteoclast differentiation and down regulated the osteoclast marker genes including C-FOS and NFATC1 in vitro. Mechanically, FT-A inhibited RANKL induced NF-kappa B signaling via suppressing the degradation of I kappa B alpha and phosphorylation of P65. Thus, FT-A might be a promising drug in treating osteoporosis.