Lobelia chinensis extract suppresses osteoclast differentiation through dual inhibition of JNK/nF-κB and btk/PLCγ2 pathways.

Osteoporosis is characterized by excessive bone resorption due to aberrant osteoclast activation. This study investigated the effects of Lobelia chinensis extract (L.C.) on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. L.C. significantly inhibited TRAP-positive multinucleated osteoclast formation from bone marrow-derived macrophages without cytotoxicity. Mechanistically, L.C. suppressed RANKL-induced phosphorylation of JNK, IκB, Btk, and PLCγ2, but not p38 or Akt, leading to down regulation of c-Fos, NFATc1, and osteoclast-specific genes (Trap, Oscar, Dcstamp, Itgb3, Atp6v0d2, Ctsk). L.C. did not affect mature osteoclasts function, indicating stage-specific inhibition. These findings suggest that L.C. as a potential anti-resorptive agent for osteoporosis.