5-caffeoylquinic acid and caffeic acid down-regulate the oxidative stress- and TNF-α-induced secretion of interleukin-8 from caco-2 cells

被引:66
作者
Zhao, Zhaohui [1 ]
Shin, Hee Soon [1 ]
Satsu, Hideo [1 ]
Totsuka, Mamoru [1 ]
Shimizu, Makoto [1 ]
机构
[1] Univ Tokyo, Dept Appl Biol Chem, Grad Sch Agr & Life Sci, Bunkyo Ku, Tokyo 1138657, Japan
关键词
chlorogenic acid; caffeic acid; IL-8; anti-inflammatory; Caco-2; intestinal epithelium;
D O I
10.1021/jf073168d
中图分类号
S [农业科学];
学科分类号
09 [农学];
摘要
Although chlorogenic acid (CHA) easily reaches a millimolar level in the gastrointestinal tract because of its high concentration in coffee and fruits, its effects on intestinal epithelial cells have been little reported. We investigated in this study the down-regulative effects of 5-caffeoylquinic acid (CQA), the predominant isomer of CHA, on the H2O2- or TNF-alpha-induced secretion of interleukin (IL)-8, a central pro-inflammatory chemokine involved in the pathogenesis of inflammatory bowel diseases, in human intestinal epithelial Caco-2 cells. After the cells had been pre- and simultaneously treated with CQA, the oversecretion of IL-8 and overexpression of its mRNA induced by H2O2 were significantly suppressed in a dose-dependent manner in the range of 0.25-2.00 mmol/L. We further found that a metabolite of CQA, caffeic acid (CA), but not, quinic acid, significantly inhibited the H2O2-induced IL-8 secretion and its mRNA expression in the same dose-dependent manner. Both CQA and CA suppressed the TNF-alpha-induced IL-8 secretion as well. Caffeic acid at 2.00 mmol/l was able to absolutely block the H2O2- or TNF-alpha-induced oversecretion of IL-8 in Caco-2 cells. However, CQA and CA did not suppress the TNF-alpha-induced increase in the IL-8 mRNA expression, indicating that the suppressive mechanisms are different between TNF-alpha-induced and H2O2-induced IL-8 production models. These results suggest that the habit of drinking coffee and/or eating fruits with a high CHA content may be beneficial to humans in preventing the genesis of inflammatory bowel diseases.
引用
收藏
页码:3863 / 3868
页数:6
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