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KMID : 1237720100430040310
Anatomy & Cell Biology
2010 Volume.43 No. 4 p.310 ~ p.316
Amorphigenin inhibits Osteoclast differentiation by suppressing c-Fos and nuclear factor of activated T cells
Kim Bong-Gyu

Kwak Han-Bok
Choi Eun-Yong
Kim Hun-Soo
Kim Myung-Hee
Kim Seong-Hwan
Choi Min-Kyu
Chun Churl-Hong
Oh Jae-Min
Kim Jeong-Joong
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-¥êB 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.
KEYWORD
Osteoporosis, Osteoclast, NFATc1
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