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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 6914514, 11 pages
Research Article

Anti-Inflammatory Potential of Carpomitra costata Ethanolic Extracts via Inhibition of NF-κB and AP-1 Activation in LPS-Stimulated RAW264.7 Macrophages

1National Marine Biodiversity Institute of Korea, Seocheon 33662, Republic of Korea
2Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, Republic of Korea
3Department of Biomedical Engineering and Center for Marine-Integrated Biomedical Technology (BK21 Plus), Pukyong National University, Busan 48513, Republic of Korea
4Department of Microbiology and Immunology, Inje University College of Medicine, Busan 49267, Republic of Korea
5Division of Endocrinology and Metabolism, Department of Internal Medicine, Dong-Eui Medical Center, Busan 47223, Republic of Korea
6Department of Radiation Oncology, College of Medicine, Kosin University, Busan 47392, Republic of Korea

Correspondence should be addressed to Il-Whan Choi; moc.liamg@amihic and Sun Young Ma; ten.liamnah@ysmoom

Received 5 October 2017; Revised 6 December 2017; Accepted 17 December 2017; Published 26 February 2018

Academic Editor: Junqing Yang

Copyright © 2018 Mi-Jin Yim 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.


Marine algae have valuable health and dietary benefits. The present study aimed to investigate whether an ethanol extract of Carpomitra costata (CCE) could inhibit the inflammatory response to LPS. CCE attenuated the production of proinflammatory mediators, such as prostaglandin E2 (PGE2) and nitric oxide (NO), by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-induced RAW264.7 macrophages. CCE also inhibited the expression of proinflammatory cytokines such as IL-1β, TNF-α, and IL-6. CCE suppressed the LPS-induced DNA-binding activity of (NF-κB) and activator protein-1 (AP-1). In addition, CCE attenuated the LPS-stimulated phosphorylation of c-Jun N-terminal kinase/stress-activated protein kinase (JNK) and phosphatidylinositol 3′-kinase/Akt (PI3K/Akt). Functional aspects of the JNK and Akt signaling pathways were analyzed using specific inhibitors, which attenuated the LPS-induced production of proinflammatory cytokines, and NO and PGE2 expression by suppressing AP-1 and NF-κB activity. In particular, the AP-1 signaling pathway is not involved in the production of inflammatory cytokines, such as IL-6, TNF-α, and IL-1β. These results suggested that CCE might exert its anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through JNK and Akt signaling pathways. The current study suggested that CCE might be a valuable candidate for the treatment of inflammatory disorders.