Orally Administered CLA Ameliorates DSS-Induced Colitis in Mice via Intestinal Barrier Improvement, Oxidative Stress Reduction, and Inflammatory Cytokine and Gut Microbiota Modulation

被引:151
作者
Chen, Yang [1 ,2 ]
Yang, Bo [1 ,2 ,4 ]
Ross, R. Paul [4 ,6 ]
Jin, Yan [10 ]
Stanton, Catherine [4 ,5 ,6 ]
Zhao, Jianxin [1 ,2 ,4 ]
Zhang, Hao [1 ,2 ,4 ,8 ,9 ]
Chen, Wei [1 ,2 ,3 ,7 ]
机构
[1] Jiangnan Univ, State Key Lab Food Sci & Technol, Wuxi 214122, Jiangsu, Peoples R China
[2] Jiangnan Univ, Sch Food Sci & Technol, Wuxi 214122, Jiangsu, Peoples R China
[3] Jiangnan Univ, Natl Engn Res Ctr Funct Food, Wuxi 214122, Jiangsu, Peoples R China
[4] Jiangnan Univ, Int Joint Res Ctr Probiot & Gut Hlth, Wuxi 214122, Jiangsu, Peoples R China
[5] Teagasc Food Res Ctr, Moorepk, Fermoy P61 C996, Cork, Ireland
[6] Univ Coll Cork, APC Microbiome Ireland, Cork T12 K8AF, Ireland
[7] Beijing Technol & Business Univ, Beijing Innovat Ctr Food Nutr & Human Hlth, Beijing 100048, Peoples R China
[8] Wuxi Translat Med Res Ctr, Wuxi 214122, Jiangsu, Peoples R China
[9] Jiangsu Translat Med Res Inst, Wuxi Branch, Wuxi 214122, Jiangsu, Peoples R China
[10] Nanjing Med Univ, Dept Gastroenterol, Affiliated Wuxi Peoples Hosp 2, Wuxi 214023, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
conjugated linoleic acid; colitis; intestinal barrier function; oxidative stress; gut microbiota; CONJUGATED LINOLEIC-ACID; GAMMA PPAR-GAMMA; NF-KAPPA-B; GENE-EXPRESSION; EPITHELIAL BARRIER; BOWEL DISEASES; FAT; BIFIDOBACTERIUM; ACTIVATION; CELLS;
D O I
10.1021/acs.jafc.9b05744
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
Dietary supplementation with conjugated linoleic acid (CLA) has been reported to alleviate the effect of colitis in mice, but the mechanisms involved need further exploration. The study aimed to investigate how orally administered CLA alleviates dextran sulfate sodium (DSS)-induced colitis in mice. CLA was administered in five different doses: 40, 20, 10, 5, and 2.5 mg/day. Doses of CLA at 10 mg/day and higher alleviated colitis symptoms and reduced inflammation induced by DSS, in which 40, 20, and 10 mg/day CLA significantly increased the concentration of mucin2 and goblet cells, but neither 5 mg/day CLA nor 2.5 mg/day CLA had any effects. Meanwhile, 40 and 20 mg/day CLA treatments significantly upregulated the concentration of tight junction proteins (ZO-1, occludin, and claudin-3) and ameliorated epithelial apoptosis caused by DSS. Moreover, oxidative-stress-related enzymes (superoxide dismutase, glutathione peroxidase, and catalase) and inflammatory cytokines [tumor necrosis factor-a, interleukin (IL)-10, and IL-6] were modulated by 40 and 20 mg/day CLA. Furthermore, 40 mg/day CLA rebalanced the gut microbiota damaged by DSS, including reducing Bacteroides and increasing Bifidobacterium and Odoribacter. In conclusion, CLA supplementation alleviated DSS-induced colitis in a dose-dependent manner by modulating inflammatory cytokines and oxidation stress, maintaining the mucosal barrier, and reverting microbiota changes.
引用
收藏
页码:13282 / 13298
页数:17
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