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丁酸盐对人肠道上皮细胞促炎通路的调节作用。

Butyrate modulating effects on pro-inflammatory pathways in human intestinal epithelial cells.

机构信息

1 Dipartimento di Scienze Umanistiche, Università Telematica Pegaso, Piazza Trieste e Trento, 48, 80132 Naples, Italy.

2 CEINGE-Biotecnologie avanzate, Via Gaetano Salvatore 486, Naples 80145, Italy.

出版信息

Benef Microbes. 2017 Oct 13;8(5):841-847. doi: 10.3920/BM2016.0197. Epub 2017 Aug 31.

Abstract

Butyrate acts as energy source for intestinal epithelial cells and as key mediator of several immune processes, modulating gene expression mainly through histone deacetylation inhibition. Thanks to these effects, butyrate has been proposed for the treatment of many intestinal diseases. Aim of this study was to investigate the effect of butyrate on the expression of a large series of target genes encoding proteins involved in pro-inflammatory pathways. We performed quantitative real-time-PCR analysis of the expression of 86 genes encoding proteins bearing to pro-inflammatory pathways, before and after butyrate exposure, in primary epithelial cells derived from human small intestine and colon. Butyrate significantly down-regulated the expression of genes involved in inflammatory response, among which nuclear factor kappa beta, interferon-gamma, Toll like 2 receptor and tumour necrosis factor-alpha. Further confirmations of these data, including studies at protein level, would support the use of butyrate as effective therapeutic strategy in intestinal inflammatory disorders.

摘要

丁酸盐可作为肠上皮细胞的能量来源,并作为多种免疫过程的关键介质,主要通过抑制组蛋白脱乙酰基来调节基因表达。由于这些作用,丁酸盐已被提议用于治疗许多肠道疾病。本研究旨在研究丁酸盐对参与促炎途径的一系列编码蛋白的靶基因表达的影响。我们在源自人小肠和结肠的原代上皮细胞中,在丁酸盐暴露前后,通过定量实时 PCR 分析了 86 个编码参与促炎途径的蛋白的基因的表达。丁酸盐显著地下调了炎症反应相关基因的表达,其中包括核因子 kappa beta、干扰素-γ、Toll 样 2 受体和肿瘤坏死因子-α。这些数据的进一步证实,包括在蛋白质水平上的研究,将支持丁酸盐作为治疗肠道炎症性疾病的有效治疗策略。

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