School of Pharmaceutical Sciences (Shenzhen), Sun Yat-sen University, Guangzhou, China.
School of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou, China.
J Gastroenterol Hepatol. 2019 Sep;34(9):1554-1562. doi: 10.1111/jgh.14583. Epub 2019 Jan 31.
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.
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.
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.
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.
炎症性肠病是由具有遗传易感性的个体对肠道微生物菌群的免疫反应失调引起的。本研究旨在确定含有山药多糖和菊粉的复合多糖(CP)对 2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎大鼠模型的影响,并从肠道微生物群落组成和功能方面解释其机制。
雄性 SD 大鼠分为三组:对照组、模型组和 CP 组。分析疾病活动指数、血清髓过氧化物酶水平以及肠道微生物群落的组成和功能。
本研究的数据表明 CP 减轻了 TNBS 诱导的大鼠结肠炎模型的炎症,并改善了实验性结肠炎。结果还表明,CP 不仅逆转了 TNBS 诱导的肠道菌群失调-以增加的短链脂肪酸(SCFAs)产生菌、乳酸产生菌和减少拟杆菌、变形菌以及硫酸盐还原菌为指标,而且还将结肠炎大鼠失调的微生物群落功能恢复到正常状态,包括改善基础代谢和减少氧化应激、细胞运动、信号转导、外源生物降解和代谢以及发病过程。
复合多糖通过调节肠道微生物群落组成和功能谱改善了 TNBS 诱导的大鼠实验性结肠炎,使其有可能作为益生菌剂用于治疗结肠炎个体的肠道菌群失调。