Ethyl acetate fraction from Cudrania Tricuspidata inhibits IL-1β-stimulated osteoclast differentiation through downregulation of MAPKs, c-Fos and NFATc1open access
- Authors
- Lee, E.-G.; Yun, H.-J.; Lee, S.-I.; Yoo, W.-H.
- Issue Date
- 2010
- Keywords
- Cell differentiation; Interleukin-1beta; Osteoclast; RANK ligand
- Citation
- Korean Journal of Internal Medicine, v.25, no.1, pp 93 - 100
- Pages
- 8
- Indexed
- SCOPUS
KCI
- Journal Title
- Korean Journal of Internal Medicine
- Volume
- 25
- Number
- 1
- Start Page
- 93
- End Page
- 100
- URI
- https://scholarworks.gnu.ac.kr/handle/sw.gnu/25989
- DOI
- 10.3904/kjim.2010.25.1.93
- ISSN
- 1226-3303
2005-6648
- Abstract
- Background/Aims: The present study was performed to determine the effects of the ethyl acetate extract of Cudrania tricuspidata (EACT) on interleukin (IL)-1β-stimulated receptor activator of NF-κB ligand (RANKL)-mediated osteoclast differentiation. Methods: Bone marrow cells were harvested from 6-week-old male imprinting control region mice, and the differentiation of osteoclasts from these cells was evaluated by tartrate-resistant acid phosphatase and resorption pit formation assay. Phosphorylated extracellular signal regulated kinase (p-ERK), phosphorylated p38, phosphorylated c-Jun amino-terminal kinase, NF-κB (p65), IκBα, c-Fos, and nuclear factor of activated Tcells c1 (NFATc1) expression was examined by immunoblotting and quantitative reverse transcription-polymerase chain reaction. Results: EACT inhibits IL-1β-stimulated RANKL-mediated osteoclast differentiation. EACT also inhibits IL-1β-stimulated RANKL-mediated phosphorylation of ERK 1/2, p38 mitogen activated protein kinase, and expression of c-Fos and NFATc1. Conclusions: These results suggest that EACT may be involved in the inhibition of bone loss by preventing osteoclast formation and may be used to manage bone destruction in inflammatory diseases, such as rheumatoid arthritis.
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