posted on 2024-02-15, 04:04authored byYu-Hong Yang, Chen Chen, Yan Zheng, Zi-Jian Wu, Meng-Qing Zhou, Xiao-Yong Liu, Kazuo Miyashita, De-Lin Duan, Lei Du
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-κB
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.