Open AccessCorilagin suppresses RANKL‐induced osteoclastogenesis and inhibits oestrogen deficiency‐induced bone loss via the NF‐κB and PI3K/AKT signalling pathways
Author(s) -
Lu Jinwei,
Ye Chenyi,
Huang Yanyong,
Huang Donghui,
Tang Lan,
Hou Weiduo,
Kuang Zhihui,
Chen Yazhou,
Xiao Shining,
Yishake Mumingjiang,
He Rongxin
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15657
Subject(s) - osteoclast , bone resorption , pi3k/akt/mtor pathway , rankl , protein kinase b , chemistry , pharmacology , nf κb , microbiology and biotechnology , cancer research , biochemistry , signal transduction , biology , activator (genetics) , endocrinology , in vitro , receptor
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.