Sargassum fusiforme polysaccharide activates nuclear factor kappa-B (NF-κB) and induces cytokine production via Toll-like receptors

被引：45
|
作者：
Chen, Xiaoming [1 ,2 ]
Yu, Guoqing [1 ,2 ]
Fan, Sairong [1 ]
Bian, Manman [1 ,2 ]
Ma, Huijun [1 ,2 ]
Lu, Jianxin [1 ,2 ]
Jin, Liqin [1 ,2 ]
机构：
[1] Wenzhou Med Univ, Sch Lab Med & Life Sci, Inst Glycobiol Engn, Wenzhou 325035, Peoples R China
[2] Wenzhou Med Univ, Sch Lab Med & Life Sci, Minist Educ China, Key Lab Lab Med, Wenzhou 325035, Peoples R China
来源：
CARBOHYDRATE POLYMERS | 2014年 / 105卷
基金：
中国国家自然科学基金;
关键词：
Sargassum fusiforme; Polysaccharide; Immunomodulatory; Toll-like receptor; NF-kappa B; INNATE IMMUNE-RESPONSE; SIGNALING PATHWAYS; CAPSULAR POLYSACCHARIDE; NITRIC-OXIDE; MACROPHAGES; INFLAMMATION; CELLS; MICE;
D O I：
10.1016/j.carbpol.2014.01.056
中图分类号：
O69 [应用化学];
学科分类号：
081704 ;
摘要：
This study was designed to investigate the mechanism of macrophage activation by the Sargassum fusiforme polysaccharide (SFPS). As a result, SFPS significantly enhanced cytokines and nitric oxide (NO) productions in peritoneal macrophages, and stimulated macrophages to produce the cytokines and NO through the induction of their genes expression. The pretreatment of peritoneal macrophages with special antibodies [Toll-like receptors (TLRs) antibody] significantly blocked SFPS-induced tumor necrosis factor alpha (TNF-alpha) and NO production. Furthermore, pyrrolidine dithiocarbamate (PDTC), a specific inhibitor of NF-kappa B, effectively suppressed SFPS-induced TNF-a and interleukin 1 beta (IL-1 beta) secretion in peritoneal macrophages, indicating that SFPS stimulated macrophages to produce cytokines through the NF-kappa B pathway and the result was further confirmed by the experiment of Western blotting (WB) and confocal laser scanning microscope (CLSM). Taken together, these results suggest that SFPS-mediated induction of cytokines and NO production in macrophages is mediated, at least in part, by TLRs/NF-kappa B signaling pathway. (C) 2014 Elsevier Ltd. All rights reserved.
引用
收藏
页码：113 / 120
页数：8
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