Amorphigenin inhibits Osteoclast differentiation by suppressing c-Fos and nuclear factor of activated T cells.
10.5115/acb.2010.43.4.310
- Author:
Bong Gyu KIM
1
;
Han Bok KWAK
;
Eun Yong CHOI
;
Hun Soo KIM
;
Myung Hee KIM
;
Seong Hwan KIM
;
Min Kyu CHOI
;
Churl Hong CHUN
;
Jaemin OH
;
Jeong Joong KIM
Author Information
1. Department of Orthopedic Surgery, School of Medicine, Wonkwang University, Iksan, Korea.
- Publication Type:In Vitro ; Original Article
- Keywords:
Osteoporosis;
Osteoclast;
NFATc1
- MeSH:
Bone Marrow;
Down-Regulation;
Femur;
Inflammation;
Macrophages;
NF-kappa B;
Osteoclasts;
Osteoporosis;
Rotenone;
T-Lymphocytes
- From:Anatomy & Cell Biology
2010;43(4):310-316
- CountryRepublic of Korea
- Language:English
-
Abstract:
Among the several rotenoids, amorphigenin is isolated from the leaves of Amopha Fruticosa and it is known that has anti-proliferative effects and anti-cnacer effects in many cell types. The main aim of this study was to investigate the effects of amorphigenin on osteoclast differentiation in vitro and on LPS treated inflammatory bone loss model in vivo. We show here that amorphigenin inhibited RANKL-induced osteoclast differentiation from bone marrow macrophages in a dose dependent manner without cellular toxicity. Anti-osteoclastogenic properties of amorphigenin were based on a down-regulation of c-fos and NFATc1. Amorphigenin markedly inhibited RANKL-induced p38 and NF-kappaB pathways, but other pathways were not affected. Micro-CT analysis of the femurs showed that amorphigenin protected the LPS-induced bone loss. We concluded that amorphigenin can prevent inflammation-induced bone loss. Thus we expect that amorphigenin could be a treatment option for bone erosion caused by inflammation.
