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Asiatic acid  is a triterpenoid compound extracted from a medicinal plant  Centella asiatica . It has been used as a highly efficient compound for the treatment of cancer and hyperlipidemia, as well as possessing potential antiinflammatory properties. However, its effects on bone metabolism and osteoporosis haven’t been reported. The purpose of our research were to reveal the biomolecular effects of  asiatic acid  on osteoclasts, and its underlying molecular mechanisms regulating its effects on receptor activator of NF-κB ligand (RANKL)-induced signaling pathways. We found that  asiatic acid  inhibited multinucleated tartrate-resistant acid phosphatase (TRAcP)-positive osteoclast differentiation and osteoclast induced bone loss. Real time PCR showed that  asiatic acid  reduced the expression of down-cascade target genes including  Ctsk ,  Nfatc1 ,  Calcr , and  Atp6v0d2 . Western blot and luciferase reporter gene assays revealed that  asiatic acid  inhibits RANKL mediated NF-κB and NFATc1 signalings. Further,  in vivo  study demonstrated  asiatic acid  attenuates estrogen deficiency-induced bone loss in ovariectomized mice. MicroCT and histology analyses revealed that osteoclast numbers were significantly suppressed in  asiatic acid  treated groups. Furthermore, serum levels of TRAcP and CTX-1 were downregulated in treated groups. Taken together, our data show that  asiatic acid  can inhibit osteoclastic formation and reduce OVX-induced bone resorption through RANKL-activated NF-κB or NFATc1 signaling, suggesting that  asiatic acid  may be a potential and effective natural compound for the therapy of excessive RANKL-related osteolytic diseases.

Asiatic Acid Inhibits OVX-Induced Osteoporosis and Osteoclastogenesis Via Regulating RANKL-Mediated NF-κb and Nfatc1 Signaling Pathways