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黄芩多糖通过改善肠道屏障功能和调节肠道微生物群来改善 DSS 诱导的溃疡性结肠炎。

Scutellaria baicalensis Georgi polysaccharide ameliorates DSS-induced ulcerative colitis by improving intestinal barrier function and modulating gut microbiota.

机构信息

Affliated Hospital of Integrated Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210028, Jiangsu, PR China.

School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, Jiangsu, PR China.

出版信息

Int J Biol Macromol. 2021 Jan 1;166:1035-1045. doi: 10.1016/j.ijbiomac.2020.10.259. Epub 2020 Nov 4.

Abstract

The aim of this study was to investigate the effect of a polysaccharide from Scutellaria baicalensis Georgi on UC. Gut microbiota dysbiosis is a worldwide problem associating with ulcerative colitis. One homogeneous polysaccharide, named SP2-1, was isolated from Scutellaria baicalensis Georgi. SP2-1 comprised mannose, ribose, rhamnose, glucuronic acid, glucose, xylose, arabinose, fucose in the molar ratio of 5.06:21.24:1.00:20.25:3.49:50.90:228.77:2.40, with Mw of 3.72 × 10 Da. SP2-1 treatment attenuated body weight loss, reduced DAI, ameliorated colonic pathological damage, and decreased MPO activity of UC mice induced by DSS. SP2-1 also suppressed the levels of proinflammatory cytokines. Additionally, the intestinal barrier was repaired due to the up-regulated expressions of ZO-1, Occludin and Claudin-5. SP2-1 remarkably enhanced the levels of acetic acid, propionic acid, and butyric acid in DSS-treated mice. Furthermore, as compared with model group, the abundance of Firmicutes, Bifidobacterium, Lactobacillus, and Roseburia were significantly increased with SP2-1 treatment. And SP2-1 could significantly inhibit the levels of Bacteroides, Proteobacteria and Staphylococcus. In conclusion, SP2-1 might serve as a novel drug candidate against UC.

摘要

本研究旨在探讨黄芩多糖对溃疡性结肠炎(UC)的作用。肠道微生物失调是一个全球性问题,与溃疡性结肠炎有关。从黄芩中分离得到一种均一多糖,命名为 SP2-1。SP2-1 由甘露糖、核糖、鼠李糖、葡萄糖醛酸、葡萄糖、木糖、阿拉伯糖、岩藻糖和果糖以摩尔比 5.06:21.24:1.00:20.25:3.49:50.90:228.77:2.40 组成,Mw 为 3.72×10 Da。SP2-1 治疗可减轻体重减轻,降低 DAI,改善结肠病理损伤,并降低 DSS 诱导的 UC 小鼠的 MPO 活性。SP2-1 还抑制促炎细胞因子水平。此外,由于 ZO-1、Occludin 和 Claudin-5 的表达上调,肠道屏障得到修复。SP2-1 显著提高了 DSS 处理小鼠中乙酸、丙酸和丁酸的水平。此外,与模型组相比,SP2-1 治疗可显著增加厚壁菌门、双歧杆菌、乳杆菌和罗斯伯里氏菌的丰度,而显著抑制拟杆菌、变形菌和葡萄球菌的水平。总之,SP2-1 可能是一种治疗 UC 的新型候选药物。

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