4.7 Article

Dietary supplementation with high dose of epigallocatechin-3-gallate promotes inflammatory response in mice

期刊

JOURNAL OF NUTRITIONAL BIOCHEMISTRY
卷 23, 期 6, 页码 526-531

出版社

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jnutbio.2011.02.006

关键词

Green tea; EGCG; Inflammation; Splenocytes; Macrophages

资金

  1. US Department of Agriculture, National Institute of Food and Agriculture [2010-65200-20360]
  2. US Department of Agriculture, Agriculture Research Service [58-1950-7-707]

向作者/读者索取更多资源

Epigallocatechin-3-gallate (EGCG) from green tea has been indicated to have anti-inflammatory activity. However, most of the evidence is in vitro studies in which EGCG is often added at levels unachievable by oral intake. With few exceptions, in vivo studies along this line have been conducted in animal models of diseases, and the results are inconclusive. In this study, we fed C57BL/6 mice a diet containing 0%, 0.15%, 0.3% or 1% (w/w) EGCG for 6 weeks. Contrary to the assumption that EGCG would reduce inflammatory response, mice fed 0.15% and 0.3% EGCG diet exhibited no change while those fed 1% EGCG diet produced more proinflammatory cytokines tumor necrosis factor-alpha, interleukin (IL)-beta, and 1L-1 beta and lipid inflammatory mediator prostaglandin E-2 in their splenocytes and macrophages (M Phi) and less IL-4 in splenocytes. Spleens from the mice fed 1% EGCG diet also had higher proportions of regulatory T cells, M Phi, natural killer (NK) cells and NKT cells compared to those from mice fed the other diets. These results suggest that high intake of EGCG may induce a proinflammatory response, and this change may be associated with a disturbed homeostasis of immune cells involving changes in both function and number of specific immune cell populations. While the mechanisms and clinical significance for this effect of EGCG remain to be investigated further, these data suggest the need for defining accurate EGCG dose limits to induce an anti-inflammatory effect since current data indicate that higher doses would produce an inflammatory response. (C) 2012 Elsevier Inc. All rights reserved.

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