Shaanxi Engineering Laboratory for Food Green Processing and Safety Control and Shaanxi Key Laboratory for Hazard Factors Assessment in Processing and Storage of Agricultural Products, College of Food Engineering and Nutritional Science, Shaanxi Normal University, Xi'an 710119, China.
J Agric Food Chem. 2024 Oct 30;72(43):23859-23874. doi: 10.1021/acs.jafc.4c06435. Epub 2024 Oct 21.
A previous study showed that kiwifruit polysaccharide (KFP) has benefits in relieving intestinal inflammation, while the underlying mechanism remains unresolved. The objective of this study was to investigate the regulatory effect of KFP on the gut microbiota metabolism and intestinal barrier of ulcerative colitis (UC) mice induced by dextran sulfate sodium (DSS). KFP significantly improved the UC symptoms including weight loss, shortened colon length, splenomegaly, diarrhea, hematochezia, and colon inflammation of mice. In addition, KFP could alleviate DSS-caused gut microbiota dysbiosis and increase the levels of short-chain fatty acids in the cecal contents of mice. Furthermore, the results of nontargeted and targeted metabolomics analysis combined with antibiotic treatment revealed that KFP could regulate gut microbiota-dependent tryptophan metabolism, activate the aryl hydrocarbon receptor (AhR) in colon cells, and enhance interleukin-22 production and tight junction proteins' (ZO-1, occludin, and claudin3) expression to repair the intestinal barrier in UC mice. Immunofluorescence results showed that KFP significantly upregulated the conjunction of lectin WGA and UEA1 in the UC mouse colon, implying that KFP promoted fucosylation in the colon. These results suggest that KFP alleviates UC primarily via targeting the gut microbiota involved in the AhR pathway and upregulating colon fucosylation.
先前的研究表明，猕猴桃多糖（KFP）在缓解肠道炎症方面具有益处，但其潜在机制尚不清楚。本研究旨在探讨 KFP 对葡聚糖硫酸钠（DSS）诱导的溃疡性结肠炎（UC）小鼠肠道微生物群代谢和肠道屏障的调节作用。KFP 显著改善了 UC 症状，包括体重减轻、结肠缩短、脾肿大、腹泻、血便和结肠炎症。此外，KFP 可以减轻 DSS 引起的肠道微生物群失调，并增加小鼠盲肠内容物中短链脂肪酸的水平。此外，非靶向和靶向代谢组学分析结合抗生素处理的结果表明，KFP 可以调节肠道微生物群依赖的色氨酸代谢，激活结肠细胞中的芳香烃受体（AhR），并增强白细胞介素-22 的产生和紧密连接蛋白（ZO-1、occludin 和 claudin3）的表达，从而修复 UC 小鼠的肠道屏障。免疫荧光结果表明，KFP 显著上调了 UC 小鼠结肠中凝集素 WGA 和 UEA1 的结合，这表明 KFP 促进了结肠中的岩藻糖基化。这些结果表明，KFP 通过靶向参与 AhR 途径的肠道微生物群并上调结肠岩藻糖基化来缓解 UC。
