Fucoxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis and Gut Microbiota Dysbiosis in Mice

被引:10
作者
Yang, Yu-Hong [1 ,2 ]
Chen, Chen [3 ,4 ]
Zheng, Yan [5 ]
Wu, Zi-Jian [3 ,4 ]
Zhou, Meng-Qing [3 ]
Liu, Xiao-Yong [2 ]
Miyashita, Kazuo [6 ]
Duan, De-Lin [7 ,8 ]
Du, Lei [3 ,4 ]
机构
[1] Qilu Univ Technol, Shandong Acad Sci, Sch Food Sci & Engn, Jinan 250353, Shandong, Peoples R China
[2] Shandong Haizhibao Ocean Sci & Technol Co Ltd, Rongcheng City 264300, Shandong, Peoples R China
[3] Shandong Univ, Cheeloo Coll Med, Sch Publ Hlth, Dept Nutr & Food Hyg, Jinan 250012, Shandong, Peoples R China
[4] Shandong Univ, Jinan Cent Hosp, Res Ctr Translat Med, Jinan 250013, Shandong, Peoples R China
[5] Shandong First Med Univ, Res Ctr Translat Med, Cent Hosp, Jinan 250013, Shandong, Peoples R China
[6] Obihiro Univ Agr & Vet Med, Ctr Ind Univ Collaborat, Obihiro, Hokkaido 0808555, Japan
[7] Chinese Acad Sci, Key Lab Breeding Biotechnol & Sustainable Aquacult, Shandong Prov Key Lab Expt Marine Biol, Inst Oceanol, Qingdao 266071, Shandong, Peoples R China
[8] Qingdao Natl Lab Marine Sci & Technol, Lab Marine Biol & Biotechnol, Qingdao 266237, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
fucoxanthin; colitis; intestinal barrier function; anti-inflammation; antioxidation; gut microbiota; NF-KAPPA-B; INTESTINAL BARRIER; OXIDATIVE STRESS; ULCERATIVE-COLITIS; MECHANISMS; IBD; APOPTOSIS;
D O I
10.1021/acs.jafc.3c08811
中图分类号
S [农业科学];
学科分类号
09 ;
摘要
The purpose of this study was to evaluate the preventive role and underlying mechanisms of fucoxanthin (Fx) on dextran sulfate sodium (DSS)-induced colitis in mice. The present data demonstrated that oral administration of Fx (50 and 200 mg/kg body weight/day) for 36 days significantly alleviated the severity of colitis in DSS-treated mice, as evidenced by attenuating body weight loss, bloody stool, diarrhea, shortened colon length, colonic epithelium distortion, a thin mucus layer, goblet cell depletion, damaged crypts, and extensive infiltration of inflammatory cells in the colonic mucosa. Additionally, Fx notably relieved DSS-induced intestinal epithelial barrier dysfunction via maintaining the tight junction function and preventing excessive apoptosis of colonic epithelial cells. Moreover, Fx effectively diminished colonic inflammation and oxidative stress in DSS-treated mice, and its mechanisms might be due to blunting the activation of NF-kappa B and NLRP3 inflammasome signaling pathways. Furthermore, Fx also modulates DSS-induced gut microbiota dysbiosis via recovering the richness and diversity of gut microbiota and reshaping the structure of gut microbiota, such as increasing the Firmicutes and Bacteroidota (F/B) ratio and elevating the relative abundance of some potential beneficial bacteria, including Lactobacillaceae and Lachnospiraceae. Overall, Fx might be developed as a promising functional ingredient to prevent colitis and maintain intestinal homeostasis.
引用
收藏
页码:4142 / 4154
页数:13
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