Attenuation of iNOS and COX2 by blueberry polyphenols is mediated through the suppression of NF-κB activation

被引:60
|
作者
Lau, Francis C. [1 ]
Joseph, James A. [1 ]
McDonald, Jane E. [2 ]
Kalt, Wilhelmina [2 ]
机构
[1] Tufts Univ, USDA, Human Nutr Res Ctr Aging, Boston, MA 02111 USA
[2] Agr & Agri Food Canada, Atlantic Food & Hort Res Ctr, Kentville, NS B4N 1J5, Canada
关键词
Blueberries; Polyphenols; Anti-inflammation; Inducible nitric oxide synthase; Cyclooxygenase; 2; Nuclear factor-kappa B; NITRIC-OXIDE PRODUCTION; OXIDATIVE STRESS; INFLAMMATORY MECHANISMS; GENE-EXPRESSION; MICROGLIA; FLAVONOIDS; CELLS; FRUIT; PROGRESSION; CYTOKINES;
D O I
10.1016/j.jff.2009.05.001
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Treatment of BV2 microglial cells with blueberry extracts has been shown to be effective in reducing lipopolysaccharide (LPS)-induced proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), inducible NO synthase (iNOS), and cyclooxygenase 2 (COX2). The current study explored the possibility that the down-regulation of iNOS and COX2 by blueberry extracts was mediated through NF-kappa B signaling pathway. A column-purified fraction of polyphenol-enriched blueberry extract (PC18) was used to treat LPS-activated BV2 cells. The results thus far showed that blueberry polyphenols significantly suppressed iNOS and COX2 promoter activities. In addition, blueberry polyphenols inhibited NF-kappa B nuclear translocation in LPS-activated BV2 cells. These findings suggested that the beneficial effects of blueberries may involve direct modulation of oxidative stress and/or inflammatory signaling cascades. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:274 / 283
页数:10
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