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Compound polysaccharides ameliorate experimental colitis by modulating gut microbiota composition and function

机译:通过调节肠道微生物群组成和功能来改善实验性结肠炎的复合多糖

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摘要

Abstract Background and Aim Inflammatory bowel disease results from a dysregulated immune response to intestinal microbial flora in individuals with genetic predisposition(s). This study aimed to determine the effects of compound polysaccharides (CP) containing yam polysaccharide and inulin on the rat model of colitis induced by 2,4,6‐trinitrobenzenesulfonic acid (TNBS) and to explain the mechanism in terms of gut microbiota composition and function. Methods Male SD rats were divided into three groups: the control group, the model group, and the CP group. Disease activity index, serum myeloperoxidase level, and the composition and function of gut microbiota were analyzed. Results The data in the study showed CP reduced inflammation in the rat model of colitis induced by TNBS and ameliorated the experimental colitis. The results also indicated that CP not only reversed TNBS‐induced gut dysbiosis‐indexed by increased short‐chain fatty acids (SCFAs)‐producing bacteria, lactic acid‐producing bacteria, and decreased Bacteroides, Proteobacteria as well as sulfate‐reducing bacteria, but also restored the dysregulated microbiota function of colitic rats into a normal condition, including an improvement on basic metabolism and a reduction on oxidative stress, cell motility, signal transduction, xenobiotics biodegradation, and metabolism as well as pathogenesis processes. Conclusions Compound polysaccharides ameliorated the experimental colitis of rats induced by TNBS by modulating the gut microbiota composition and function profiles, which makes it possible to be used as prebiotic agents to treat gut dysbiosis in colitis individuals.
机译:摘要背景和目标炎症性肠病导致具有遗传易感性肠道微生物植物的肠道微生物植物的失调免疫菌。本研究旨在确定含铝多糖和菊粉的复合多糖(CP)对2,4,6-三硝基苯磺酸(TNB)诱导的结肠炎大鼠模型的影响,并在肠道微生物酵母组合物和功能方面解释机制。方法将雄性SD大鼠分为三组:对照组,模型组和CP组。分析了疾病活动指数,血清髓氧化酶水平,肠道微生物酶的组成和功能。结果研究中的数据显示CP在TNB诱导的结肠炎大鼠模型中降低炎症并改善实验性结肠炎。结果还表明,CP不仅通过增加的短链脂肪酸(SCFA) - 发霉的细菌,乳酸产生细菌和降低的菌斑,促菌细菌以及硫酸盐还原细菌,CP不仅逆转了TNBS诱导的肠道诱导肠道诱导的肠道诱导肠道诱导肠道诱导肠道诱导肠道挛缩症。还恢复了粘土大鼠的失餐的微生物A功能,进入正常条件,包括改善基本代谢,氧化应激,细胞运动,信号转导,异种术生物降解以及代谢以及发病过程的含量。结论化合物多糖通过调节肠道微生物组成和功能谱来改善由TNB诱导的大鼠的实验性结肠炎,这使得可以用作益生元剂来治疗结肠炎个体中的肠道脱泻。

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  • 作者单位

    School of Pharmaceutical Sciences (Shenzhen)Sun Yat‐sen UniversityGuangzhou China;

    School of Pharmaceutical Sciences (Shenzhen)Sun Yat‐sen UniversityGuangzhou China;

    School of Chinese Materia MedicaGuangzhou University of Chinese MedicineGuangzhou China;

    School of Pharmaceutical SciencesSun Yat‐sen UniversityGuangzhou China;

    School of Pharmaceutical Sciences (Shenzhen)Sun Yat‐sen UniversityGuangzhou China;

    School of Pharmaceutical Sciences (Shenzhen)Sun Yat‐sen UniversityGuangzhou China;

    School of Pharmaceutical SciencesSun Yat‐sen UniversityGuangzhou China;

    School of Chinese Materia MedicaGuangzhou University of Chinese MedicineGuangzhou China;

    School of Pharmaceutical SciencesSun Yat‐sen UniversityGuangzhou China;

    School of Chinese Materia MedicaGuangzhou University of Chinese MedicineGuangzhou China;

    School of Pharmaceutical Sciences (Shenzhen)Sun Yat‐sen UniversityGuangzhou China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 消化系及腹部疾病;
  • 关键词

    compound polysaccharides; function prediction; gut microbiome; inflammatory bowel disease;

    机译:复合多糖;功能预测;肠道微生物组;炎症性肠病;

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