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水果提取物通过调节肠道微生物群、炎症介质和细胞因子缓解 DSS 诱导的溃疡性结肠炎。

Fruit Extract Alleviates DSS-Induced Ulcerative Colitis by Regulating Gut Microbiota, Inflammatory Mediators, and Cytokines.

机构信息

Key Laboratory of Fermentation Engineering (Ministry of Education), Cooperative Innovation Center of Industrial Fermentation (Ministry of Education & Hubei Province), School of Biological Engineering and Food, Hubei University of Technology, Wuhan 430068, China.

出版信息

Molecules. 2023 Jul 31;28(15):5783. doi: 10.3390/molecules28155783.

DOI:10.3390/molecules28155783
PMID:37570753
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10421151/
Abstract

Ulcerative colitis (UC) is a chronic inflammatory disease significantly impacting patients' lives. This study aimed to elucidate the alleviating effect of ethyl acetate extract (TBEA) from fruit on UC and to explore its mechanism. TBEA was the fraction with the best anti-inflammatory activity screened using in vitro anti-inflammatory assays, and HPLC initially characterized its composition. The mice model of ulcerative colitis was established after free drinking of 2.5% dextran sulfate sodium for six days, and the experimental group was treated with 50 mg/kg and 100 mg/kg TBEA for seven days. We found that TBEA significantly alleviated symptoms in UC mice, including a physiologically significant reduction in disease activity index and pathological damage to colonic tissue. TBEA dramatically slowed down oxidative stress and inflammatory process in UC mice, as evidenced by decreasing myeloperoxidase and malondialdehyde activities and increasing glutathione and catalase levels by reducing the concentrations of IL-6, IL-1β, TNF-α, and NO in UC mice, as well as by regulating key proteins in the IL-6/JAK2/STAT3 pathway. Meanwhile, TBEA maintained intestinal homeostasis by regulating intestinal flora structure. Our study provides new ideas for developing TBEA into a new drug to treat UC.

摘要

溃疡性结肠炎(UC)是一种严重影响患者生活的慢性炎症性疾病。本研究旨在阐明 果实的乙酸乙酯提取物(TBEA)对溃疡性结肠炎的缓解作用,并探讨其机制。TBEA 是通过体外抗炎试验筛选出的抗炎活性最佳的馏分,并用 HPLC 初步对其组成进行了表征。在自由饮用 2.5%葡聚糖硫酸钠六天后,建立了溃疡性结肠炎小鼠模型,实验组用 50mg/kg 和 100mg/kg TBEA 治疗七天。我们发现 TBEA 显著缓解了 UC 小鼠的症状,包括疾病活动指数的生理性显著降低和结肠组织的病理损伤。TBEA 通过降低 UC 小鼠中 IL-6、IL-1β、TNF-α 和 NO 的浓度,以及调节 IL-6/JAK2/STAT3 通路中的关键蛋白,显著减缓了 UC 小鼠的氧化应激和炎症过程,同时还通过降低髓过氧化物酶和丙二醛的活性以及增加谷胱甘肽和过氧化氢酶的水平来实现。此外,TBEA 通过调节肠道菌群结构维持肠道内环境稳态。我们的研究为将 TBEA 开发成治疗 UC 的新药提供了新的思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b7c/10421151/b2ac42582a4b/molecules-28-05783-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b7c/10421151/8592fc3f34e9/molecules-28-05783-g008.jpg
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