Searchable abstracts of presentations at key conferences on calcified tissues
Bone Abstracts (2014) 3 PP163 | DOI: 10.1530/boneabs.3.PP163

ECTS2014 Poster Presentations Cell biology: osteoclasts and bone resorption (22 abstracts)

The molecular mechanism of n-butanol extracts of Panax notoginseng on RANKL-induced osteoclastogenesis in RAW264.7 cells

Hyo-In Hwang , Young-Joo Jang & Seon-Yle Ko

Dankook University, Cheonan-so, Choongnam-do, Republic of Korea.

This study examined the anti-osteoclastogenic effect of n-butanol extracts of Panax notoginseng on the receptor activator of NF-kB ligand (RANKL) induced RAW264.7 cells. Panax notoginseng is commonly used to treat chronic liver disease. Notoginseng has many beneficial effects, such as the suppression of liver fibrosis and anti-cancer activities. Notoginseng contains several biologically active components, such as ginsenosides Rb1, Rg1, Rd and Re and notoginsenoside R1.The effects of n-butanol extract of Panax notoginseng (bPN) on osteoclasts were examined by measuring the following: the cell viability, the formation of tartrate-resistant acid phosphatase (TRAP) (+) multinucleated cells, RANK/RANKL signaling pathways and mRNA expression of osteoclast-associated genes. bPN inhibited the formation of RANKL-stimulated TRAP (+) multinucleated cells. bPN also inhibited the RANKL-stimulated activation of ERK signaling, and inhibited the RANKL-stimulated degradation of I?B in the RAW264.7 cells. In addition, the RANKL-stimulated induction of NFATc1 transcription factors was abrogated by bPN. bPN decreased the mRNA expression of osteoclast-associated genes, including TRAP and cathepsin K in the RAW264.7 cells. Our data demonstrate that bPN inhibits osteoclastogenesis by inhibiting RANKL-induced activation of signaling molecules and transcription factor in osteoclast precursors.

Volume 3

European Calcified Tissue Society Congress 2014

Prague, Czech Republic
17 May 2014 - 20 May 2014

European Calcified Tissue Society 

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