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논문 기본 정보

자료유형
학술저널
저자정보
Ryu, BoMi (School of Pharmacy, The University of Queensland) Choi, Il-Whan (Department of Microbiology, College of Medicine and Advanced Research Center for Multiple Myeloma, Inje University) Qian, Zhong-Ji (College of Food Science and Technology, Guangdong Ocean University) Heo, Soo-Jin (Global Bioresources Research Center, Korea Institute of Ocean Science and Technology) Kang, Do-Hyung (Global Bioresources Research Center, Korea Institute of Ocean Science and Technology) Oh, Chulhong (Global Bioresources Research Center, Korea Institute of Ocean Science and Technology) Jeon, You-Jin (Department of Marine Life Sciences, Jeju National University) Jang, Chul Ho (Department of Otolaryngology, Chonnam National University Medical School) Park, Won Sun (Department of Physiology, School of Medicine, Kangwon National University) Kang, Kyong-Hwa (Department of Marine-bio Convergence Science, Pukyong National University) Je, Jae-Young (Department of Marine-bio Convergence Science, Pukyong National University) Kim, Se-Kwon (Department of Marine-bio Convergence Science, Pukyong National University) Kim, Young-Mog (Department of Food Science and Technology, Pukyong National) Ko, Seok-Chun Kim, GeunHyung Jung, Won-Kyo
저널정보
한국조류학회(藻類) Algae Algae 제29권 제4호
발행연도
2014.1
수록면
343 - 353 (11page)

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Despite the extensive literature on marine algae over the past few decades, a paucity of published research and studies exists on red algae. The purpose of this study was to evaluate the potential therapeutic properties of the ethanol extract of the red alga Callophyllis japonica against lipopolysaccharide (LPS)-stimulated macrophage inflammation. The C. japonica extract (CJE) significantly inhibited the nitric oxide (NO) production and the induced dose-dependent reduction of the protein and mRNA levels of inducible nitric oxide synthase and cyclooxygenase-2. Additionally, the CJE reduced the mRNA levels of inflammatory cytokines, including tumor necrosis factor-${\alpha}$, interleukin (IL)-$1{\beta}$, and IL-6. We investigated the mechanism by which the CJE inhibits NO by examining the level of mitogen-activated protein kinases (MAPKs) activation, which is an inflammation-induced signaling pathway in macrophages. The CJE significantly suppressed the LPS-induced phosphorylation of c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38 MAPK. Taken together, the results of this study demonstrate that the CJE inhibits LPS-induced inflammation by blocking the MAPK pathway in macrophages.

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