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BioMed Research International
Volume 2014, Article ID 329712, 10 pages
Research Article

Anti-Inflammatory Effects of Siegesbeckia orientalis Ethanol Extract in In Vitro and In Vivo Models

1Department of Nutrition, I-Shou University, Kaohsiung 82445, Taiwan
2Institute of Biotechnology and Chemical Engineering, I-Shou University, Kaohsiung 84001, Taiwan
3Department of Obstetrics and Gynecology, E-DA Hospital, I-Shou University, Kaohsiung 82445, Taiwan
4Division of Cardiology, E-DA Hospital, I-Shou University, Kaohsiung 82445, Taiwan
5Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, E-DA Hospital, I-Shou University, Kaohsiung 82445, Taiwan

Received 4 April 2014; Revised 12 July 2014; Accepted 21 July 2014; Published 26 August 2014

Academic Editor: Chia-Chien Hsieh

Copyright © 2014 Yong-Han Hong 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.


This study aims to investigate the anti-inflammatory responses and mechanisms of Siegesbeckia orientalis ethanol extract (SOE). In cell culture experiments, RAW264.7 cells were pretreated with SOE and stimulated with lipopolysaccharide (LPS) for inflammatory mediators assay. In animal experiments, mice were tube-fed with SOE for 1 week, and s.c. injected with λ-carrageenan or i.p. injected with LPS to simulate inflammation. The degree of paw edema was assessed, and cytokine profile in sera and mouse survival were recorded. Data showed that SOE significantly reduced NO, IL-6, and TNF-α production in LPS-stimulated RAW264.7 cells. In vivo studies demonstrated that mice supplemented with 32 mg SOE/kg BW/day significantly lowered sera IL-6 level and resulted a higher survival rate compared to the control group (). Furthermore, SOE inhibited LPS-induced NF-κB activation by blocking the degradation of IκB-α. The SOE also reduced significantly the phosphorylation of ERK1/2, p38, and JNK in a dose-dependent manner. In summary, the in vitro and in vivo evidence indicate that SOE can attenuate acute inflammation by inhibiting inflammatory mediators via suppression of MAPKs- and NF-κB-dependent pathways.