Open AccessDracorhodin perchlorate inhibits osteoclastogenesis through repressing RANKL‐stimulated NFATc1 activity
Author(s) -
Liu Yuhao,
Wang Ziyi,
Ma Chao,
Wei Zhenquan,
Chen Kai,
Wang Chao,
Zhou Chi,
Chen Leilei,
Zhang Qingwen,
Chen Zhenqiu,
He Wei,
Xu Jiake
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.15003
Subject(s) - osteoclast , rankl , chemistry , microbiology and biotechnology , osteoblast , runx2 , nf κb , cancer research , bone resorption , osteoporosis , function (biology) , signal transduction , medicine , endocrinology , gene , biochemistry , biology , activator (genetics) , receptor , in vitro
Osteolytic skeletal disorders are caused by an imbalance in the osteoclast and osteoblast function. Suppressing the differentiation and resorptive function of osteoclast is a key strategy for treating osteolytic diseases. Dracorhodin perchlorate (D.P), an active component from dragon blood resin, has been used for facilitating wound healing and anti‐cancer treatments. In this study, we determined the effect of D.P on osteoclast differentiation and function. We have found that D.P inhibited RANKL‐induced osteoclast formation and resorbed pits of hydroxyapatite‐coated plate in a dose‐dependent manner. D.P also disrupted the formation of intact actin‐rich podosome structures in mature osteoclasts and inhibited osteoclast‐specific gene and protein expressions. Further, D.P was able to suppress RANKL‐activated JNK, NF‐κB and Ca 2+ signalling pathways and reduces the expression level of NFATc1 as well as the nucleus translocation of NFATc1. Overall, these results indicated a potential therapeutic effect of D.P on osteoclast‐related conditions.