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Mediators of Inflammation
Volume 2013, Article ID 761506, 11 pages
Research Article

Extracellular Signal-Regulated Kinase Is a Direct Target of the Anti-Inflammatory Compound Amentoflavone Derived from Torreya nucifera

1Department of Genetic Engineering, Sungkyunkwan University, Suwon 440-746, Republic of Korea
2Medical Beauty Research Institute, AmorePacific R&D Center, Yongin 446-729, Republic of Korea
3Department of Dermatological Health Management, College of Health Science, Eulji University, Seongnam 461-713, Republic of Korea
4College of Biomedical Sciences, Kangwon National University, Chuncheon 200-701, Republic of Korea
5College of Natural Sciences, Kangwon National University, Chuncheon 200-701, Republic of Korea

Received 8 April 2013; Accepted 24 June 2013

Academic Editor: Hidde Bult

Copyright © 2013 Jueun Oh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Amentoflavone is a biflavonoid compound with antioxidant, anticancer, antibacterial, antiviral, anti-inflammatory, and UV-blocking activities that can be isolated from Torreya nucifera, Biophytum sensitivum, and Selaginella tamariscina. In this study, the molecular mechanism underlying amentoflavone’s anti-inflammatory activity was investigated. Amentoflavone dose dependently suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW264.7 cells stimulated with the TLR4 ligand lipopolysaccharide (LPS; derived from Gram-negative bacteria). Amentoflavone suppressed the nuclear translocation of c-Fos, a subunit of activator protein (AP)-1, at 60 min after LPS stimulation and inhibited the activity of purified and immunoprecipitated extracellular signal-regulated kinase (ERK), which mediates c-Fos translocation. In agreement with these results, amentoflavone also suppressed the formation of a molecular complex including ERK and c-Fos. Therefore, our data strongly suggest that amentoflavone’s immunopharmacological activities are due to its direct effect on ERK.