Exopolysaccharides Produced by Bifidobacterium longum subsp. longum YS108R Ameliorates DSS-Induced Ulcerative Colitis in Mice by Improving the Gut Barrier and Regulating the Gut Microbiota.
Huizhen LiHaitao LiCatherine StantonR Paul RossJianxin ZhaoJianxin ZhaoChen WeiPublished in: Journal of agricultural and food chemistry (2024)
Ulcerative colitis (UC) is a major disease that has endangered human health. Our previous study demonstrated that Bifidobacterium longum subsp. longum YS108R, a ropy exopolysaccharide (EPS)-producing bacterium, could alleviate UC in mice, but it is unclear whether EPS is the key substance responsible for its action. In this study, we proposed to investigate the remitting effect of EPS from B. longum subsp. longum YS108R on UC in a DSS-induced UC mouse model. Water extraction and alcohol precipitation were applied to extract EPS from the supernatant of B. longum subsp. longum YS108R culture. Then the animal trial was performed, and the results indicated that YS108R EPS ameliorated colonic pathological damage and the intestinal barrier. YS108R EPS suppressed inflammation via NF-κB signaling pathway inhibition and attenuated oxidative stress via the Nrf2 signaling pathway activation. Remarkably, YS108R EPS regulated gut microbiota, as evidenced by an increase in short-chain fatty acid (SCFA)-producing bacteria and a decline in Gram-negative bacteria, resulting in an increase of propionate and butyrate and a reduction of lipopolysaccharide (LPS). Collectively, YS108R EPS manipulated the intestinal microbiota and its metabolites, which further improved the intestinal barrier and inhibited inflammation and oxidative stress, thereby alleviating UC.
Keyphrases
- oxidative stress
- diabetic rats
- signaling pathway
- ulcerative colitis
- induced apoptosis
- mouse model
- human health
- ischemia reperfusion injury
- risk assessment
- multiple sclerosis
- pi k akt
- high glucose
- clinical trial
- inflammatory response
- transcription factor
- randomized controlled trial
- climate change
- immune response
- study protocol
- endothelial cells
- drug induced
- type diabetes
- phase ii
- toll like receptor
- insulin resistance
- anti inflammatory