Fucoxanthin Alleviates Dextran Sulfate Sodium-Induced Colitis and Gut Microbiota Dysbiosis in Mice.
Yu-Hong YangChen ChenYan ZhengZi-Jian WuMeng-Qing ZhouXiao-Yong LiuKazuo MiyashitaDe-Lin DuanLei DuPublished in: Journal of agricultural and food chemistry (2024)
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.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- ulcerative colitis
- high fat diet induced
- body weight
- nlrp inflammasome
- signaling pathway
- weight loss
- cell cycle arrest
- dna damage
- endoplasmic reticulum stress
- high glucose
- bariatric surgery
- type diabetes
- cell death
- cell therapy
- wild type
- metabolic syndrome
- drug induced
- toll like receptor
- adipose tissue
- cell proliferation
- electronic health record
- physical activity
- artificial intelligence
- antibiotic resistance genes
- clostridium difficile