miR-155下调Ets-1参与溃疡性结肠炎的发病机制

发布时间：2018-05-12 01:25

本文选题：溃疡性结肠炎 + miR-　；参考：《中药新药与临床药理》2015年03期

【摘要】：目的探讨miR-155在溃疡性结肠炎(UC)中的作用机制。方法构建miR-155高表达溃疡性结肠炎小鼠模型,并进一步采用Western blot方法检测外周血白细胞转录调节因子-1(EST-1)及Th17相关炎症因子蛋白表达。结果在UC模型组,miR-155基因转染后小鼠外周血白细胞中miR-155表达量较对照显著升高,且与UC结肠炎症程度呈正相关;UC模型组小鼠外周血白细胞中Est-1呈低表达,而Th17相关细胞因子(IL-17、IL-23及IL-6)呈相对高表达;miR-155转染后,UC小鼠这种变化趋势更加显著,Est-1表达更低,而IL-17、IL-23及IL-6表达更高。结论 miR-155通过抑制Ets-1表达,进而促进Th17相关炎症因子分泌参与溃疡性结肠炎的发病。
[Abstract]:Objective to investigate the mechanism of miR-155 in ulcerative colitis (UC). Methods the mouse model of ulcerative colitis with high expression of miR-155 was established, and the expression of transcription regulatory factor -1 (EST-1) and Th17 related inflammatory factor protein (Th17) in peripheral blood leukocytes were detected by Western blot method. Results the expression of miR-155 in peripheral blood leukocytes of UC model group was significantly higher than that of control group, and it was positively correlated with the degree of UC colitis. The expression of Est-1 in peripheral blood leukocytes of UC model group was lower than that of control group. However, the expression of IL-17 IL-23 and IL-6) in Th17 related cytokines was significantly lower in UCU mice after transfection with miR-155, but the expression of IL-17, IL-23 and IL-6 was higher in UCU mice. Conclusion miR-155 inhibits the expression of Ets-1 and promotes the secretion of Th17 related inflammatory factors in the pathogenesis of ulcerative colitis.
【作者单位】：广州中医药大学第一附属医院;
【基金】：广东省科技计划项目(2012B031800483)
【分类号】：R574.62

【参考文献】