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通过调节肠道微生物群-胆酸途径保护肠道上皮并减轻结肠炎炎症。

Protects the Intestinal Epithelium and Mitigates Inflammation in Colitis via Regulating the Gut Microbiota-Cholic Acid Pathway.

机构信息

School of Light Industry and Food Engineering, Guangxi University, Nanning 530004, China.

出版信息

J Agric Food Chem. 2024 Feb 21;72(7):3572-3583. doi: 10.1021/acs.jafc.3c08527. Epub 2024 Feb 9.

Abstract

In this study, we aimed to explore the protective effects of in colitis mice and the potential mechanisms. Results showed that () effectively colonized the intestinal tract and alleviated colitis symptoms by reducing the disease activity index. Moreover, mitigated intestinal epithelial cell damage, inhibited the pro-inflammatory factors, and upregulated tight junction (TJ)-proteins. Gut microbiota and metabolome analysis found that boosted bile acid-regulating genera (such as and 1), which promoted bile acid deconjugation in the intestine. Notably, cholic acid (CA) was closely associated with the expression levels of inflammatory factors and TJ-proteins ( < 0.05). Our in vitro cell experiments further confirmed that CA (20.24 ± 4.53 pg/mL) contributed to the inhibition of lipopolysaccharide-induced tumor necrosis factor-α expression (49.32 ± 5.27 pg/mL) and enhanced the expression of TJ-proteins (Occludin and Claudin-1) and MUC2. This study suggested that could be a probiotic candidate for use in infant foods.

摘要

在这项研究中,我们旨在探讨 在结肠炎小鼠中的保护作用及其潜在机制。结果表明, ()有效地定植于肠道,并通过降低疾病活动指数来缓解结肠炎症状。此外, 减轻了肠道上皮细胞损伤,抑制了促炎因子,并上调了紧密连接(TJ)蛋白。肠道微生物组和代谢组学分析发现, 促进了胆汁酸调节属(如 和 1)的生长,从而促进了肠道中胆汁酸的去结合。值得注意的是,胆酸(CA)与炎症因子和 TJ 蛋白的表达水平密切相关(<0.05)。我们的体外细胞实验进一步证实,CA(20.24±4.53 pg/mL)有助于抑制脂多糖诱导的肿瘤坏死因子-α表达(49.32±5.27 pg/mL),并增强 TJ 蛋白(Occludin 和 Claudin-1)和 MUC2 的表达。本研究表明, 可能成为婴幼儿食品中使用的益生菌候选物。

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