Clostridium butyricum ameliorates ulcerative colitis in mice by regulating intestinal microbiota and enhancing autophagy
10.3760/cma.j.cn112309-20241116-00392
- VernacularTitle:丁酸梭菌通过调节肠道菌群并提高自噬水平改善小鼠溃疡性结肠炎
- Author:
Lu MEI
1
;
Ye ZHAO
;
Yilian GUO
;
Yiqing GUO
;
Huang HUANG
;
Yong YU
;
Yang MI
;
Pengyuan ZHENG
Author Information
1. 郑州大学第五附属医院消化内科，郑州450052
- Publication Type:Journal Article
- Keywords:
Intestinal microbiota;
Autophagy;
Clostridium butyricum;
Ulcerative colitis
- From:
Chinese Journal of Microbiology and Immunology
2025;45(10):860-868
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of Clostridium butyricum on ulcerative colitis（UC）in mice and its impact on gut microbiota and autophagy levels. Methods:Eighteen C57BL/6J mice were randomly divided into a control group，a model group，and a treatment group，with six mice in each group using simple random sampling. Mice in the model and treatment groups were freely given 2.5% dextran sulfate sodium salt（DSS）solution for 5 days to establish a UC model. After successful modeling，the control and model groups were gavaged with PBS，while the treatment group was gavaged with 5×10 8 CFU/ml of live Clostridium butyricum. After the intervention，changes in body weight，disease activity index（DAI），colonic length，and pathological conditions were compared among the groups. Fluorescence quantitative PCR was used to detect the expression levels of intestinal inflammatory cytokines IL-1β and TNF-α. Myeloperoxidase（MPO）levels were analyzed，and Western blot was employed to detect the expression levels of zonula occludens-1（ZO-1），Occludin，LC3Ⅱ/LC3I，p62，and AMP-activated protein kinase/mammalian target of rapamycin AMPK/mTOR proteins. High-throughput sequencing technology was utilized to analyze the intestinal microbiota of the mice. Results:Compared with mice in the control group，the mice in the model group exhibited significant weight loss，markedly increased DAI and inflammation levels（ P<0.01），destruction of colonic structure，decreased expression levels of intestinal tight junction proteins（ P<0.05），suppressed autophagy levels（ P<0.05），and dysbiosis of the intestinal microbiota. In contrast，mice in the treatment group had a slower weight decline compared to the model group（ P<0.000 1），reduced DAI（ P<0.01），down-regulated inflammation levels（ P<0.01），improved barrier function（ P<0.05），up-regulated autophagy levels（ P<0.01），and an improved intestinal microbiota composition. Conclusions:Clostridium butyricum may ameliorate UC by modulating the intestinal microbiota composition，and enhancing autophagy levels，thus improving intestinal barrier function and inhibiting inflammatory progression in UC mice.
