京尼平
兰克尔
破骨细胞
医学
癌症研究
骨吸收
内科学
药理学
内分泌学
细胞生物学
生物化学
化学
受体
生物
激活剂(遗传学)
壳聚糖
作者
Chang Hoon Lee,J.-Y. Kim,Jaemin Oh,Wan‐Hee Yoo,S.-H. Beak,Jung-Won Choi,W.-S. Lee,M.-S. Lee
标识
DOI:10.1136/annrheumdis-2014-eular.2308
摘要
Background
People over the age of 50 are at risk of osteoporotic fracture, which may lead to increased morbidity and mortality. Osteoclasts are responsible for bone resorption in bone-related disorders. Genipin is a well-known geniposide aglycon derived from Gardenia jasminoides, which has long been used in oriental medicine for controlling diverse conditions such as inflammation and infection. Objectives
We aimed to evaluate the effects of genipin on RANKL-induced osteoclast differentiation and its mechanism of action. Results
Genipin dose-dependently inhibited early stage RANKL-induced osteoclast differentiation in bone marrow macrophages (BMMs) during culture. Genipin inhibited RANKL-induced IκB degradation and suppressed the mRNA expression of osteoclastic markers such as NFATc1, TRAP, and OSCAR in RANKL-treated BMMs, but did not affect c-Fos mRNA expression. Interestingly, genipin markedly inhibited c-Fos protein expression in BMMs, which was reversed in the presence of the proteosome inhibitor MG-132. Furthermore, genipin inhibited RANKL-mediated osteoclast differentiation, which was also rescued by overexpression of c-Fos and NFATc1 in BMMs. Conclusions
Taken together, our findings indicate that genipin down-regulated RANKL-induced osteoclast differentiation through inhibition of c-Fos protein proteolysis as well as inhibition of IκB degradation. Our findings indicate that genipin could be a useful drug candidate that lacks toxic side effects for the treatment of osteoporosis. Disclosure of Interest
None declared DOI
10.1136/annrheumdis-2014-eular.2308
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