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低聚糖通过调节葡聚糖硫酸钠诱导的小鼠肠道微生物群和肠道代谢产物改善溃疡性结肠炎。

Oligosaccharides Improve Ulcerative Colitis by Regulating Gut Microbiota and Intestinal Metabolites in Dextran Sulfate Sodium-Induced Mice.

作者信息

Zhu Tianxiang, Hu Baifei, Ye Cheng, Hu Haiming, Yin Mingzhu, Zhang Zhigang, Li Shuiqing, Liu Yanju, Liu Hongtao

机构信息

College of Basic Medicine, Hubei University of Chinese Medicine, Wuhan, China.

Wuhan Customs Technology Center, Wuhan, China.

出版信息

Front Pharmacol. 2022 Apr 25;13:867525. doi: 10.3389/fphar.2022.867525. eCollection 2022.

Abstract

This study aimed to elucidate the mechanism of oligosaccharides (BO) in the treatment of ulcerative colitis (UC). A UC mouse model was induced by 3% Dextran sodium sulfate (DSS), and BO (200 mg/kg/d) were administered for intervention. The results show that BO effectively inhibited the release of intestinal inflammatory cytokines such as IL-6, TNF-α, and IL-1β. Also, BO profoundly elevated the secretion of mucins and the expression of tight junction (TJ) proteins to attenuate dysfunction of the intestinal barrier. The 16S rDNA sequencing and liquid chromatography/gas chromatography-mass spectrometer (LC/GC-MS) analysis of mouse feces revealed that BO regulated the disturbance of gut microbiota and intestinal metabolites. By using the fermentation broth of BO and gut microbiota-depleted mice treated with antibiotics, we confirmed the protection of BO against UC. In conclusion, BO played a role in improving UC by modulating gut microbial composition and intestinal metabolites, which provided new therapeutic strategies for UC treatment.

摘要

本研究旨在阐明低聚糖(BO)治疗溃疡性结肠炎(UC)的机制。采用3%葡聚糖硫酸钠(DSS)诱导建立UC小鼠模型,并给予BO(200mg/kg/d)进行干预。结果表明,BO能有效抑制IL-6、TNF-α和IL-1β等肠道炎性细胞因子的释放。此外,BO还能显著提高黏蛋白的分泌和紧密连接(TJ)蛋白的表达,以减轻肠道屏障功能障碍。对小鼠粪便进行16S rDNA测序和液相色谱/气相色谱-质谱联用仪(LC/GC-MS)分析发现,BO可调节肠道微生物群和肠道代谢产物的紊乱。通过使用BO发酵液和用抗生素处理的肠道微生物群耗竭小鼠,我们证实了BO对UC的保护作用。总之,BO通过调节肠道微生物组成和肠道代谢产物在改善UC中发挥作用,为UC治疗提供了新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9e97/9081565/ff51e33506f9/fphar-13-867525-g001.jpg

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