康普茶多糖通过调节肠道微生物群和重塑新陈代谢途径缓解小鼠 DSS 引起的结肠炎

Zhong-Hao Ji, Wen-Yin Xie, Pei-Sen Zhao, W. Ren, Hong-Juan Jin, Bao Yuan
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摘要

溃疡性结肠炎(UC)是无法治愈的疾病,合理的饮食干预对预防 UC 非常重要。昆布茶是一种发酵饮料,起源于中国,具有抗氧化、抗菌和降血糖等多种活性。本研究旨在分析康普茶多糖(KP)对 UC 的保护作用,并确定其作用机制。结果表明,KP干预能有效缓解右旋糖酐硫酸钠盐(DSS)诱导的结肠炎症状,抑制DSS诱导的炎症和氧化应激。此外,KP 还能降低肠道通透性,促进紧密连接蛋白的表达,并有助于维持鹅口疮细胞数量和促进粘液分泌。16S rDNA结果表明,KP干预增加了Rikenellaceae_RC9_gut_group和Clostridiales_unclassified的丰度。非靶向代谢组学技术显示,KP 可以逆转 DSS 引起的肠道代谢紊乱。这项研究表明,KP 通过帮助维持肠道屏障的完整性、调节肠道微生物群和重塑代谢途径,缓解了 DSS 诱导的结肠炎。这些发现为将 KP 用作预防 UC 的膳食补充剂提供了理论依据。
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Kombucha polysaccharide alleviates DSS-induced colitis in mice by modulating the gut microbiota and remodeling metabolism pathways
Ulcerative colitis (UC) is incurable, and rational dietary interventions are important in preventing UC. Kombucha is a fermented beverage that originated in China and has a variety of activities, including antioxidant, antibacterial and hypoglycemic activities. The aim of this study was to analyze the protective effect of Kombucha polysaccharide (KP) against UC and determine its mechanism of action. The results showed that KP intervention was effective in alleviating dextran sulfate sodium salt (DSS)-induced colitis symptoms and inhibiting DSS-induced inflammation and oxidative stress. Moreover, KP was able to reduce intestinal permeability, promote the expression of tight junction proteins, and help maintain thrush cell numbers and promote mucus secretion. The 16S rDNA results indicated that KP intervention increased the abundance of Rikenellaceae_RC9_gut_group and Clostridiales_unclassified. Untargeted metabolomics techniques revealed that KP can reverse DSS-induced disorders in intestinal metabolism. This study demonstrated that KP alleviated DSS-induced colitis by helping maintain intestinal barrier integrity, regulating the gut microbiota and remodeling metabolism pathways. The findings provide a theoretical basis for the application of KP as a dietary supplement for the prevention of UC.
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