The efficacy and potential mechanism of cnidium lactone to inhibit osteoclast differentiation

  • Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):3087-3093. doi: 10.1080/21691401.2019.1637881.
Jun-Yang Liang  1 ,  Wen-Liang Wu  2 ,  Yun-Xia Chen  2 ,  Haichun Liu  2
Affiliations
  • 1. a Department of Second Area of Spinal Surgery, Weihaiwei People's Hospital , Weihai , China.
  • 2. b Department of Orthopedics, Qilu Hospital of Shandong University , Jinan , China.
PMID: 31343277 DOI: 10.1080/21691401.2019.1637881
Abstract

Cnidium lactone is effective in the maintenance of bone mass in various osteoporosis models; however, the precise molecular mechanisms are not understood. In this study, we investigated the effects and underlying mechanisms of action of cnidium lactone on receptor activator of NF-κB ligand (RANKL)-induced osteoclastogenesis. Cnidium lactone dose-dependently inhibited osteoclast differentiation and formation, decreased the bone-resorbing activity of osteoclasts, and downregulated the expression of osteoclast differentiation marker genes. Cnidium lactone treatment considerably reduced RANKL-induced p38 MAPK and PI3K-Akt signal activity in RAW264.7 cells. The cnidium lactone-induced osteoclastogenesis was significantly attenuated by inhibition of p38 and PI3K through pretreatment with SB203580 and LY294002, respectively. Furthermore, cnidium lactone inhibited the expression of c-Fos and NFATc-1 with dose-dependently and enhanced by SB203580 and LY294002. In conclusion, cnidium lactone inhibits osteoclast differentiation through p38 MAPK and PI3K-Akt signalling pathway/c-Fos/NFATc1 signalling pathway.

Keywords
Cnidium lactone; PI3K-Akt signalling pathway; differentiation; osteoclast.
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