Structural characteristics and <Emphasis Type="Italic">in vitro</Emphasis> macrophage activation of acetyl fucoidan from <Emphasis Type="Italic">Cladosiphon okamuranus</Emphasis> |
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Authors: | Takeshi Teruya Hideki Tatemoto Teruko Konishi Masakuni Tako |
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Institution: | (1) The United Graduate School of Agricultural Sciences, Kagoshima University, 1-21-24, Korimoto, Kagoshima 890-0065, Japan;(2) Department of Bioproduction, University of the Ryukyus, 1, Senbaru, Nishihara, Okinawa 903-0213, Japan;(3) Department of Bioscience and Biotechnology, University of the Ryukyus, 1, Senbaru, Nishihara, Okinawa 903-0213, Japan |
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Abstract: | We investigated a structural characteristics of acetyl fucoidan (CAF) isolated from commercially cultured Cladosiphon okamuranus. The CAF-induced macrophage activation and its signaling pathways in murine macrophage cell line, RAW 264.7 were also investigated.
From the results of methylation analysis, CAF consisted of α-1→3 linked l-fucosyl residues and substituted sulfate and acetyl groups at C-4 on the main chain. CAF induced production of nitric oxide
(NO), tumor necrosis factor-α and interleukin-6 in RAW 264.7 cells. Sulfate and acetyl groups of CAF involved in CAF-induced
NO production. Neutralizing anti-Toll-like receptor 4 (TLR4), anti-CD14 and anti-scavenger receptor class A (SRA) but not
anti-complement receptor type 3 monoclonal antibodies decreased CAF-induced NO production. The results of immunoblot analysis
indicated that CAF activated mitogen-activated protein kinases (MAPKs) such as p38 MAPK, extracellular signal-regulated kinase
(ERK)1/2 and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK). SB203580 (p38 MAPK inhibitor) and SP600125 (SAPK/JNK inhibitor), but not U0126 (MAPK/ERK kinase
1/2 inhibitor) decreased CAF-induced NO production. The results suggested that CAF induced macrophage activation through membrane
receptors TLR4, CD14 and SRA, and MAPK signaling pathways. |
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