Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Avenida Antonio Carlos, 6627, Pampulha, Belo Horizonte, CEP 31270-901, MG, Brazil.
Br J Nutr. 2013 Apr 28;109(8):1396-407. doi: 10.1017/S000711451200342X. Epub 2012 Aug 20.
Tributyrin (TBT) is a TAG composed of three butyric acids that has beneficial effects on ulcerative colitis due to its trophic, anti-inflammatory, pro-apoptotic and anti-carcinogenic properties. The goal of the present study was to evaluate the efficacy and mechanisms of action of TBT supplementation in the prevention of mucosal damage in experimental colitis. Mice received either a control diet or a TBT-supplemented diet for 15 d. Colitis was induced by dextran sodium sulphate administration during the last 7 d. Mucosal damage and the activation of immune cells and cytokines were determined by histological score, flow cytometry and ELISA. Leucocyte rolling and adhesion were assessed by intravital microscopy. Oxidative stress was determined by monitoring hydroperoxide concentration and evaluating superoxide dismutase (SOD) and catalase activities. Intestinal permeability was analysed using diethylenetriaminepentaacetate acid (99mTcDTPA). Compared with the colitis group, the animals in the colitis+TBT group had reduced mucosal damage and neutrophil and eosinophil mucosal infiltration, which were associated with a higher percentage of regulatory T cells (Treg) and higher levels of transforming growth factor β and IL-10 in the lamina propria. The level of in vivo leucocyte adhesion in the colon microvasculature was reduced after TBT supplementation. A lower level of hydroperoxide and higher levels of SOD and catalase activities were associated with TBT supplementation. TBT-supplemented mice showed reduced intestinal permeability to the levels intermediate between the control and colitis groups. In conclusion, the present results show that TBT has positive effects on colonic restructuring in experimental colitis. Additionally, TBT supplementation changes the immune response by controlling inflammation and regulating the expression of anti-inflammatory cytokines and Treg.
丁三酯（TBT）是一种由三个丁酸组成的 TAG，由于其营养、抗炎、促凋亡和抗癌特性，对溃疡性结肠炎有有益的影响。本研究的目的是评估 TBT 补充剂在预防实验性结肠炎黏膜损伤中的疗效和作用机制。小鼠接受对照饮食或 TBT 补充饮食 15 天。在最后 7 天给予葡聚糖硫酸钠诱导结肠炎。通过组织学评分、流式细胞术和 ELISA 测定黏膜损伤和免疫细胞及细胞因子的激活。通过活体显微镜评估白细胞滚动和粘附。通过监测过氧化物浓度并评估超氧化物歧化酶（SOD）和过氧化氢酶活性来确定氧化应激。使用二乙三胺五乙酸（99mTcDTPA）分析肠通透性。与结肠炎组相比，结肠炎+TBT 组的动物黏膜损伤和中性粒细胞和嗜酸性粒细胞黏膜浸润减少，与固有层中调节性 T 细胞（Treg）的百分比较高以及转化生长因子 β和 IL-10 的水平较高相关。TBT 补充后，结肠微血管中体内白细胞粘附水平降低。过氧化物水平降低，SOD 和过氧化氢酶活性升高与 TBT 补充有关。TBT 补充的小鼠表现出降低的肠通透性，介于对照组和结肠炎组之间。总之，本研究结果表明 TBT 对实验性结肠炎的结肠重构有积极影响。此外，TBT 补充通过控制炎症和调节抗炎细胞因子和 Treg 的表达来改变免疫反应。
