反式茴香脑通过重塑肠道菌群以调节免疫和胆汁酸代谢来减轻DSS诱导的溃疡性结肠炎。

IF 4.4 3区 医学 Q2 CELL BIOLOGY
Mediators of Inflammation Pub Date : 2023-09-21 eCollection Date: 2023-01-01 DOI:10.1155/2023/4188510
Xu-Hui Li, Li Liu, Wen-Zhong Wu
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引用次数: 0

摘要

溃疡性结肠炎(UC)是最常见的炎症性肠病(IBD);它是无法治愈的,而且治疗费用昂贵。反式茴香脑是茴香的主要成分,具有多种生物活性。越来越多的研究证明了草药活性成分治疗UC的疗效。本研究旨在探讨TA在UC中的作用及其机制。在本研究中,我们在右旋糖酐硫酸钠盐(DSS)诱导的UC小鼠身上进行了实验。TA组灌胃62.5 mg/kg TA,在第8-14天每天灌胃一次。为了观察TA对结肠组织的影响,进行了各种研究,包括肠道屏障蛋白表达的western印迹和免疫组织化学、细胞凋亡的TUNEL染色、炎症水平的western blot和ELISA、Th17/Treg的流式细胞术、血液胆汁酸含量的LC-MS、血液脂肪酸含量的GC-MS和肠道内容物的16s RNA。TA减轻UC小鼠的体重减轻;结肠长度增加;减轻肠黏膜损伤;上调claudin-1、occludin和ZO-1蛋白表达水平;结肠和血清中炎症因子减少;并减轻细胞凋亡。TA通过抑制结肠中的集落丰度和减少Th17/Treg细胞分化来降低脂肪酸和胆汁酸水平。我们发现TA通过重塑肠道菌群来调节免疫和胆汁酸代谢,从而减轻DSS诱导的UC。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Trans-Anethole Alleviates DSS-Induced Ulcerative Colitis by Remodeling the Intestinal Flora to Regulate Immunity and Bile Acid Metabolism.

Trans-Anethole Alleviates DSS-Induced Ulcerative Colitis by Remodeling the Intestinal Flora to Regulate Immunity and Bile Acid Metabolism.

Trans-Anethole Alleviates DSS-Induced Ulcerative Colitis by Remodeling the Intestinal Flora to Regulate Immunity and Bile Acid Metabolism.

Trans-Anethole Alleviates DSS-Induced Ulcerative Colitis by Remodeling the Intestinal Flora to Regulate Immunity and Bile Acid Metabolism.

Ulcerative colitis (UC) is the most common inflammatory bowel disease (IBD); it is incurable, and the treatment is expensive. Trans-anethole (TA), the main component of fennel, exhibits various biological activities. An increasing number of studies have demonstrated the efficacy of herbal active ingredients in the treatment of UC. This study aimed to investigate the effect and mechanism of TA in UC. In this study, we have experimented on mice with dextran sulfate sodium salt (DSS)-induced UC. The TA group was gavaged with 62.5 mg/kg TA by gavage once daily on days 8-14. To observe the effect of TA on the colon tissue, various investigations were performed, including western blot and immunohistochemistry for intestinal barrier protein expression, TUNEL staining for apoptosis, western blot, and ELISA for inflammation level, flow cytometry for Th17/Treg, LC-MS for blood bile acid content, GC-MS for blood fatty acid content, and 16s RNA for intestinal contents. TA alleviated weight loss in mice with UC; increased colon length; alleviated intestinal mucosal damage; upregulated claudin-1, occludin, and ZO-1 protein expression levels; reduced inflammatory factors in the colon and serum; and alleviated apoptosis. TA reduced fatty acid and bile acid levels by inhibiting colony abundance and reducing Th17/Treg cell differentiation in the colon. We found that TA alleviates DSS-induced UC by remodeling the intestinal flora to regulate immunity and bile acid metabolism.

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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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