Protective effect of sugar cane extract against dextran sulfate sodium-induced colonic inflammation in mice

被引:7
|
作者
Wang, Bin [1 ,2 ]
Li, Yansen [1 ]
Mizu, Masami [3 ]
Furuta, Toma [3 ]
Li, ChunMei [1 ]
机构
[1] Nanjing Agr Univ, Coll Anim Sci & Technol, 1 Weigang, Nanjing 210095, Jiangsu, Peoples R China
[2] Jiangsu Food & Pharmaceut Sci Coll, Huaian 223005, Peoples R China
[3] Mitsui Sugar Co Ltd, Prod Dev Div, Tokyo 1038423, Japan
来源
TISSUE & CELL | 2017年 / 49卷 / 01期
基金
中国国家自然科学基金;
关键词
Sugar cane extract; Inflammation; Oxidative stress; Tight junction; Mouse; TIGHT JUNCTION PROTEINS; DSS-INDUCED COLITIS; KAPPA-B ACTIVATION; OXIDATIVE STRESS; ANTIOXIDANT; IBD; MODULATION; PATHWAYS; MODELS;
D O I
10.1016/j.tice.2016.12.008
中图分类号
R602 [外科病理学、解剖学]; R32 [人体形态学];
学科分类号
100101 ;
摘要
Sugar cane extract (SCE) exhibits various biological effects and has been reported to enhance animal growth performance. However, the effect of SCE on inflammation in animals is still obscure. To study the effects and underlying mechanism of SCE on dextran sulfate sodium (DSS)-induced colonic inflammation, forty female ICR mice (26.63 +/- 0.19 g, 6-week-old) were assigned into four groups: a control group (Cont), a DSS-challenged group (DSS), a SCE-supplemented group (SCE), and a DSS+ SCE group (DSS+ SCE). Mice in Cont group and DSS group were fed basic diet and other mice received 1% SCE supplemented in basic diet from 6-week to 8-week-old. Mice in DSS and DSS+ SCE groups were also given a 4% DSS solution from 7-week to 8-week-old via drinking water to induce colonic inflammation. After 2 weeks, mice were sacrificed and samples were collected. The results showed that dietary SCE alleviated DSS induced growth suppression, splenic damage, colonic histological changes, colonic inflammation, oxidative stress, and colonic dysfunction of tight junctions. Meanwhile, the DSS exposure activated nuclear transcription factor kappa B p65 and inhibited nuclear factor E2-related factor 2 (Nrf2), while SCE markedly attenuated the DSS-promoted effect on the p65 nuclear accumulation and the DSS-inhibited effect on the Nrf2 nuclear accumulation. In conclusion, SCE conferred a protective role in the DSS-induced inflammation and the mechanism might be associated with the activated signals of the nuclear factor kappa B p65 and Nrf2. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:8 / 14
页数:7
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