Camellia oil alleviates DSS-induced colitis in mice by regulating the abundance of intestinal flora and suppressing the NF-κB signaling pathway

被引:9
|
作者
Jiang, Qihong [1 ,2 ]
Jiang, Chenkai [1 ]
Lu, Hongling [1 ]
Zhou, Tianyi [1 ]
Hu, Wenjun [1 ]
Tan, Chin Ping [2 ,3 ]
Feng, Yongcai [2 ]
Shen, Guoxin [1 ]
Xiang, Xingwei [4 ]
Chen, Lin [1 ]
机构
[1] Zhejiang Acad Agr Sci, Inst Sericultural & Tea, Hangzhou 310021, Zhejiang, Peoples R China
[2] Xujing Hangzhou Biotechnol Res Inst Co Ltd, Hangzhou 310021, Zhejiang, Peoples R China
[3] Univ Putra Malaysia, Fac Food Sci & Technol, Dept Food Technol, Serdang 43400, Malaysia
[4] Zhejiang Univ Technol, Coll Food Sci & Technol, Hangzhou 310014, Zhejiang, Peoples R China
关键词
Camellia oil; Ulcerative colitis; Intestinal permeability; NF-kappa B signaling pathway; Gut microbiota; INDUCED ULCERATIVE-COLITIS; GUT MICROBIOTA; OXIDATIVE STRESS; POLYSACCHARIDE; INFLAMMATION;
D O I
10.1016/j.jff.2023.105777
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Colitis is characterized by colonic inflammation and impaired gut health, and alterations in the gut microbiota may lead to the development of inflammatory bowel disease (IBD). Camellia oil (CO) possesses high nutritional value and offers various health benefits for human metabolic disorders and diseases. However, it is unclear whether CO ameliorates IBD and plays a role in the gut microbiota. This study aimed to investigate the effect of CO on colonic inflammation and gut microbiota using a mice model of dextran sodium sulfate (Dss)-induced ulcerative colitis (UC). Our findings demonstrated that CO inhibited weight loss and colon shortening and improved intestinal barrier function. Additionally, CO treatment reduced oxidative stress and inflammatory responses in Dss-induced colitis. Furthermore, CO significantly inhibited p65 and I kappa B alpha phosphorylation and alleviated colonic inflammation. Moreover, we observed that CO treatment increased the abundance of Bacteroides, Lactobacillus, and Odoribacter, while decreasing the abundance of Alistipes, Lachnospiraceae NK4A136 group, Ruminococcaceae UCG-014, uncultured Bacteroidales bacterium, and Prevotellaceae_UCG-001. Additionally, CO treatment promoted the production of SCFAs. These data indicated the promising potential of CO to prevent UC by maintaining gut barrier function, inhibiting the NF-kappa B signaling pathway, and modulating the gut microbiota.
引用
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页数:10
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