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Journal of Chemistry
Volume 2016 (2016), Article ID 6509212, 9 pages
http://dx.doi.org/10.1155/2016/6509212
Research Article

Fucofuroeckol-A from Eisenia bicyclis Inhibits Inflammation in Lipopolysaccharide-Induced Mouse Macrophages via Downregulation of the MAPK/NF-κB Signaling Pathway

1Korea Food Research Institute, Baekhyun-dong, Seongnam, Gyeonggi 13539, Republic of Korea
2Food and Safety Research Center, National Fisheries Research & Development, Busan 46083, Republic of Korea
3Department of Chemistry, Dong-Eui University, Busan 47340, Republic of Korea
4Marine Bioprocess Research Center, Pukyong National University, Busan 48513, Republic of Korea
5Department of Specialized Graduate School Science and Technology Convergence, Pukyong National University, Busan 48547, Republic of Korea

Received 28 March 2016; Revised 16 May 2016; Accepted 25 May 2016

Academic Editor: Patricia Valentao

Copyright © 2016 Sang-Hoon Lee 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.

Abstract

Fucofuroeckol-A (FF) isolated from an edible perennial brown seaweed Eisenia bicyclis was shown to be potent anti-inflammatory agents. FF suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2) and the expression of inducible nitric oxide synthase and cyclooxygenase-2 dose dependently in lipopolysaccharide- (LPS-) induced RAW 264.7 mouse macrophages. An enzyme-linked immunosorbent assay and cytometric bead array assay demonstrated that FF significantly reduced the production of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, and that of the monocyte chemoattractant protein-1. Moreover, FF reduced the activation of nuclear factor κB (NF-κB) and mitogen-activated protein kinases (MAPKs). These results strongly suggest that the inhibitory effects of fucofuroeckol-A from E. bicyclis on LPS-induced NO and PGE2 production might be due to the suppression of the NF-κB and MAPK signaling pathway.