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长双歧杆菌对2,4,6-三硝基苯磺酸诱导的大鼠结肠炎中叉头框蛋白P3启动子甲基化水平的影响。

Bifidobacterium longum affects the methylation level of forkhead box P3 promoter in 2, 4, 6-trinitrobenzenesulphonic acid induced colitis in rats.

作者信息

Zhang Ming, Zhou Lixing, Zhang Shu, Yang Yang, Xu Lei, Hua Zichun, Zou Xiaoping

机构信息

Department of Gastroenterology, Drum Tower Hospital Affiliated to Medical School of Nanjing University, Nanjing 210008, China; Jiangsu Clinical Medical Center of Digestive Disease, China.

Department of Gastroenterology, Nanjing Medical University Affiliated Drum Tower Clinical Medical College, Nanjing 210008, China.

出版信息

Microb Pathog. 2017 Sep;110:426-430. doi: 10.1016/j.micpath.2017.07.029. Epub 2017 Jul 18.

Abstract

Bifidobacterium longum (B. Longum) is a common probiotic colonized in the human gut and against the development of chronic inflammation including inflammatory bowel disease (IBD). But the underlying mechanism remains unknown. The aim of this study was to evaluate the affection of B. longum on the methylation levels of forkhead box P3 (Foxp3) promoter. 2, 4, 6-trinitrobenzenesulphonic acid (TNBS)-induced colitis rat models were treated with B. longum or medium, respectively. The genomic DNA of spleen peripheral blood mononuclear cells (PBMC) cells was extracted. After bisulphite treatment and pyrosequencing, the methylation levels of each CpG sites in the promoter of forkhead box protein P3 (Foxp3) were analyzed. B. Longum treatment changes the methylation level in Foxp3 promoter in TNBS-treated colitis rats, and significantly demethylates several CpG sites in Foxp3 promoter. The demethylation of Foxp3 promoter might be involved in the effectiveness of B. Longum treatment for IBD. Further research remains necessary to investigate the role of B. Longum in Foxp3 demethylation. Using B. Longum or its metabolic products is an option for further investigations on potential treatments for IBD.

摘要

长双歧杆菌是一种常见的定殖于人体肠道的益生菌,可抵抗包括炎症性肠病(IBD)在内的慢性炎症的发展。但其潜在机制尚不清楚。本研究的目的是评估长双歧杆菌对叉头框蛋白P3(Foxp3)启动子甲基化水平的影响。分别用长双歧杆菌或培养基处理2,4,6-三硝基苯磺酸(TNBS)诱导的结肠炎大鼠模型。提取脾脏外周血单个核细胞(PBMC)的基因组DNA。经过亚硫酸氢盐处理和焦磷酸测序后,分析叉头框蛋白P3(Foxp3)启动子中每个CpG位点的甲基化水平。长双歧杆菌处理改变了TNBS诱导的结肠炎大鼠Foxp3启动子的甲基化水平,并使Foxp3启动子中的几个CpG位点显著去甲基化。Foxp3启动子的去甲基化可能与长双歧杆菌治疗IBD的有效性有关。有必要进一步研究长双歧杆菌在Foxp3去甲基化中的作用。使用长双歧杆菌或其代谢产物是进一步研究IBD潜在治疗方法的一种选择。

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