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Antioxidative and immunomodulatory effects of tributyrin supplementation on experimental colitis.

机译:补充三丁精对实验性结肠炎的抗氧化和免疫调节作用。

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摘要

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 beta 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
机译:Tributyrin(TBT)是由三种丁酸组成的TAG,由于具有营养,抗炎,促凋亡和抗癌的特性,因此对溃疡性结肠炎具有有益作用。本研究的目的是评估补充TBT预防实验性结肠炎粘膜损伤的功效和作用机制。小鼠接受对照饮食或补充TBT饮食15天。在最后7 d内,右旋糖酐硫酸钠诱发结肠炎。通过组织学评分,流式细胞术和ELISA确定粘膜损伤以及免疫细胞和细胞因子的活化。通过活体显微镜评估白细胞滚动和粘附。通过监测氢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。使用二亚乙基三胺五乙酸( 99mTc DTPA)分析肠道通透性。与结肠炎组相比,结肠炎+ TBT组的动物的粘膜损害以及嗜中性粒细胞和嗜酸性粒细胞的黏膜浸润减少,这与调节性T细胞(Treg)的百分比升高和转化生长因子β和IL-在固有层中有10个。补充TBT后,结肠微血管中的体内白细胞粘附水平降低。较低水平的过氧化氢和较高水平的SOD和过氧化氢酶活性与补充TBT有关。补充TBT的小鼠的肠道通透性降低至对照组和结肠炎组之间的中间水平。总之,目前的结果表明,TBT对实验性结肠炎的结肠重构具有积极作用。另外,TBT补充剂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。

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