Fucoidan Ameliorated Dextran Sulfate Sodium-Induced Ulcerative Colitis by Modulating Gut Microbiota and Bile Acid Metabolism

Abstract

Gut dysbiosis and bile acid (BA) metabolism disturbance are involved in the pathogenesis of ulcerative colitis. This study aimed to investigate the effect of fucoidan on BA metabolism and gut microbiota in dextran sulfate sodium-induced colitis mice. Our results showed that fucoidan effectively suppressed colonic inflammation and repaired the gut barrier. In addition, fucoidan increased the relative abundance of the Lachnospiraceae family, such as Turicibacter, Muribaculum, Parasutterella, and Colidextribacter, followed by an increase in short-chain fatty acids, especially in butyrate. Moreover, fucoidan modulated bile acid metabolism by elevating cholic acid, ursodeoxycholic acid, deoxycholic acid, and lithocholic acid and decreasing β-muricholic acid, which led to activation of FXR and TGR5 and further enhanced the gut barrier and suppressed colonic inflammation. Our results revealed that the effect of fucoidan alleviating colitis was largely mediated by gut microbiota, which was confirmed by the fecal transplantation experiment. Collectively, these findings provided the basis for fucoidan as a potential functional food for colitis.

Phenolics from Dendrobium officinale Leaf Ameliorate Dextran Sulfate Sodium-Induced Chronic Colitis by Regulating Gut Microbiota and Intestinal Barrier

“…Oscillospiraceae is a key bacterium in the acetate and butyrate production pathway, and DOPL treatment restored the decrease in the relative abundance of unclassified_Oscillospiraceae caused by DSS, which may be closely related to the final increase in the level of SCFAs in DOP groups. Previous reports categorized Colidextribacter as the beneficial bacterium that promotes the production of SCFAs . DOPL likely restored the supply of SCFAs by significantly increasing the relative abundance of this bacterium compared to that of the MC group.…”

Untargeted metabolomics revealed the regulatory effect of Maillard reaction products of ovalbumin with different degrees on the metabolism of colitis mice

“…36 In addition, cholic acid can combine with the farnesol X receptor (FXR) to maintain bile acid homeostasis through the gut-liver axis, while the activation of FXR can decrease the level of pro-inflammation cytokines by inhibiting the NF-κB pathways to reduce intestinal inflammation. 37 Bile acid levels were significantly decreased in the colitis mice, which may cause the inhibition of the FXR and consequently the more secretion of pro-inflammatory cytokines by immune cells, leading to inflammation in the intestine. 38 However, unlike the L-MRP group, the metabolic pathways in the H-MRP group are less related to bile acid metabolism and are mainly enriched in pathways such as ABC transporter and pyrimidine metabolism.…”

The regulatory effects of fucoidan and laminarin on functional dyspepsia mice induced by loperamide

“…FUC and LA have been reported to increase the diversity of gut microbiota in lots of animals and human studies. [51][52][53][54] The low-diverse condition of gut microbiota is associated with severe symptoms of FD. This part of results indicated the remarkable ability of FUC and LA in maintaining and enriching the balance of intestinal flora.…”