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  • 08월 28일 16시 이후 : 초록수정 불가능, 일정확인 및 검색만 가능

Inhibitory effect of ARAC on the inhibition of osteoclastogenesis in Raw 264.7 murine macrophage cells

2008년 8월 8일 17시 05분 45초
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목 <발표Ⅰ>
저자 및
김순남, 이의진1, 김명희2, 민용기3, 김성환4
한국화학연구원, Korea
1한국화학연구원 신약기반기술연구센터, Korea
2충남대학교 생화학과, Korea
3한국화학연구원 생명화학연구단, Korea
4한국화학연구원 화학유전체 연구실, Korea
Osteoclastogenesis is commonly associated with various age-related diseases such as osteoporosis and the receptor activator of nuclear factor-kB (NF-kB) ligand (RANKL) has been shown to play a critical role in osteoclastic bone resorption. With the fact that the development of anti-resorptive agents from natural substances has gained more interest in the treatment of osteoporosis, here, 680 natural compounds were evaluated whether they have a potential to suppress RANKL-induced osteoclastogenesis in RAW264.7 murine macrophage cells. Of these compounds, ARAC was identified as one of compounds inhibiting the RANKL-induced activity of tartrate-resistance acid phosphatase (TRAP). ARAC significantly inhibited the RANKL-induced TRAP activity with IC50, 1.58 ± 0.52 uM and also inhibited the formation of multinucleated osteoclast in a dose-dependent manner. In addition, it was shown to attenuate the RANKL-induced transcript levels of osteoclast specific genes, which have been known to be highly expressed in the process of osteoclastogenesis. Interestingly, ARAC was also shown to inhibit the RANKL-induced activation of mitogen-activated protein kinases. In conclusion, it suggested that ARAC could inhibit the process of osteoclastogenesis through the inhibition of RANKL-induced activation of MAPK signaling pathway.