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小米奎尼酸通过调节肠道微生物群和抑制MyD88/NF-κB信号通路缓解结肠炎。

Millet Quinic Acid Relieves Colitis by Regulating Gut Microbiota and Inhibiting MyD88/NF-κB Signaling Pathway.

作者信息

Li Sen, Zhang Ze, Luo Lei, Zhang Yu, Huang Kai, Guan Xiao

机构信息

School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China.

National Grain Industry (Urban Grain and Oil Security) Technology Innovation Center, Shanghai 200093, China.

出版信息

Foods. 2025 Jun 26;14(13):2267. doi: 10.3390/foods14132267.

Abstract

Polyphenols are compounds derived from plant-based food possessing numerous biological activities, including inhibiting oxidative stress, suppressing inflammation, and regulating gut microbiota. In this study, we investigated the effects of quinic acid, a phenolic acid from millet, on the regulation of gut microbiota and intestinal inflammation and further discussed the possible mechanism. The results showed that quinic acid could improve the microbiota composition of the feces of patients with inflammatory bowel disease (IBD) by in vitro anaerobic fermentation by increasing the abundance of beneficial genera including , , etc., and decreasing that of harmful genera like . Quinic acid treatment could alleviate the symptoms of dextran sodium sulfate (DSS)-induced colitis in mice, maintain the intestinal barrier, down-regulate the expression of inflammatory factors such as IL-1β and TNF-α, and inhibit the activation of the MyD88/NF-κB signaling pathway. In addition, quinic acid also improved the diversity of gut microbiota in mice with colitis. Furthermore, pseudo-germ-free colitis mice proved that the effect of quinic acid on intestinal inflammation was diminished after removing most gut microbiota by antibiotic treatment, suggesting that gut microbiota play important roles during the regulation of colitis by quinic acid. In a word, our study verified the regulatory effects of quinic acid on intestinal inflammation, depending on gut microbiota regulation and NF-κB signaling suppression.

摘要

多酚是一类源自植物性食物的化合物,具有多种生物活性,包括抑制氧化应激、抑制炎症以及调节肠道微生物群。在本研究中,我们研究了小米中的酚酸奎尼酸对肠道微生物群调节和肠道炎症的影响,并进一步探讨了可能的机制。结果表明,奎尼酸通过体外厌氧发酵可改善炎症性肠病(IBD)患者粪便中的微生物群组成,增加包括等有益菌属的丰度,降低如等有害菌属的丰度。奎尼酸处理可减轻葡聚糖硫酸钠(DSS)诱导的小鼠结肠炎症状,维持肠道屏障,下调IL-1β和TNF-α等炎症因子的表达,并抑制MyD88/NF-κB信号通路的激活。此外,奎尼酸还改善了结肠炎小鼠肠道微生物群的多样性。此外,无菌结肠炎小鼠证明,通过抗生素处理去除大多数肠道微生物群后,奎尼酸对肠道炎症的作用减弱,这表明肠道微生物群在奎尼酸调节结肠炎过程中发挥重要作用。总之,我们的研究证实了奎尼酸对肠道炎症的调节作用,这取决于对肠道微生物群的调节和对NF-κB信号的抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ddb/12249245/63fa2062f976/foods-14-02267-g001.jpg

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