Corilagin suppresses RANKL-induced osteoclastogenesis and inhibits oestrogen deficiency-induced bone loss via the NF-κB and PI3K/AKT signalling pathways

  • J Cell Mol Med. 2020 Sep;24(18):10444-10457. doi: 10.1111/jcmm.15657.
Jinwei Lu  1  2 ,  Chenyi Ye  1  2 ,  Yanyong Huang  1  2  3 ,  Donghui Huang  4 ,  Lan Tang  1  2 ,  Weiduo Hou  1  2 ,  Zhihui Kuang  1  2 ,  Yazhou Chen  1  2 ,  Shining Xiao  1  2 ,  Mumingjiang Yishake  5 ,  Rongxin He  1  2
Affiliations
  • 1. Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.
  • 2. Orthopedics Research Institute of Zhejiang University, Hangzhou, China.
  • 3. Department of Orthopedic Surgery, The First People's Hospital of Xiaoshan District, Hangzhou, China.
  • 4. Department of Orthopedic Surgery, Hangzhou Third Hospital, Hangzhou, China.
  • 5. Orthopedics Department, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China.
PMID: 32681612 DOI: 10.1111/jcmm.15657
Abstract

Over-activated osteoclastogenesis, which is initiated by inflammation, has been implicated in osteoporosis. Corilagin, a natural compound extracted from various medicinal herbaceous Plants, such as Cinnamomum Cassia, has antioxidant and anti-inflammatory activities. We found that Corilagin suppressed osteoclast differentiation in a dose-dependent manner, significantly decreased osteoclast-related gene expression and impaired bone resorption by osteoclasts. Moreover, phosphorylation of members of the nuclear factor-kappaB (NF-κB) and PI3K/Akt signalling pathways was reduced by Corilagin. In a murine model of osteoporosis, Corilagin inhibited osteoclast functions in vivo and restored oestrogen deficiency-induced bone loss. In conclusion, our findings suggested that Corilagin inhibited osteoclastogenesis by down-regulating the NF-κB and PI3K/Akt signalling pathways, thus showing its potential possibility for the treatment of osteoporosis.

Keywords
Corilagin; NF-κB; PI3K/AKT; RANKL; osteoclast.
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