AP-1 pathway-targeted inhibition of inflammatory responses in LPS-treated macrophages and EtOH/HCl-treated stomach by Archidendron clypearia methanol extract
- Authors
- Yang, WS[Yang, Woo Seok]; Jeong, D[Jeong, Deok]; Nam, G[Nam, Gyeongsug]; Yi, YS[Yi, Young-Su]; Yoon, DH[Yoon, Deok Hyo]; Kim, TW[Kim, Tae Woong]; Park, YC[Park, Yung Chul]; Hwang, H[Hwang, Hyunsik]; Rhee, MH[Rhee, Man Hee]; Hong, S[Hong, Sungyoul]; Cho, JY[Cho, Jae Youl]
- Issue Date
- 27-Mar-2013
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Archidendron clypearia Jack; Fabaceae; PGE(2) prod
- Citation
- JOURNAL OF ETHNOPHARMACOLOGY, v.146, no.2, pp.637 - 644
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF ETHNOPHARMACOLOGY
- Volume
- 146
- Number
- 2
- Start Page
- 637
- End Page
- 644
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/61195
- DOI
- 10.1016/j.jep.2013.01.034
- ISSN
- 0378-8741
- Abstract
- Ethnopharmacological relevance: Archidendron clypearia Jack. (Fabaceae) is a representative ethnomedicinal herbal plant prescribed for various inflammatory diseases such as pharyngolaryngitis and tonsillitis. However, the pharmacology behind this plant's anti-inflammatory properties has not been fully understood. Therefore, in this study, the anti-inflammatory mechanism of a 95% methanol extract (Ac-ME) was explored. Materials and Methods: The anti-inflammatory mechanism of Ac-ME on the AP-1 activation pathway, which plays a critical role in the production of prostaglandin (PG)E-2 in RAW264.7 cells and peritoneal macrophages and in induction of acute gastritis caused by HCl/EtOH, was investigated using immunoblotting, immuno-precipitation analyses, and reporter gene activity assays. In particular, enzyme assays and HPLC analysis were employed to identify direct target enzymes of Ac-ME and to detect active chemical components from the plant extract. Results: Ac-ME clearly reduced the nuclear levels of total and phospho-forms of c-Jun, FRA-1, and ATF-2. Consequently, this extract suppressed both the production of PGE(2) in lipopolysaccharide (LPS)-activated RAW264.7 and peritoneal macrophage cells and PGE(2)-dependent induction of gastritis lesion in stomach under EtOH/HCl exposure. Analysis of AP-1 upstream signalling revealed that the AP-1 activation pathway consisting of IRAK1, TRAF6, TAK1, MKK3/6, and p38 was predominantly inhibited by Ac-ME. Similarly, this extract directly blocked the enzyme activity of IRAK1, indicating that this enzyme is an inhibitory target of Ac-ME and is involved in the suppression of the AP-1 pathway. HPLC analysis showed that quercetin, which inhibits PGE2 production, is an active component in Ac-ME. Conclusion: Ac-ME is an ethnomedicinal remedy with an IRAK1/p38/AP-1-targeted inhibitory property. Since AP-1 is a major inflammation-inducing transcription factor, the therapeutic potential of Ac-ME in other AP-1-mediated inflammatory symptoms will be further tested. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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Collections - Biotechnology and Bioengineering > Integrative Biotechnology > 1. Journal Articles
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