miR-155在溃疡性结肠炎患者直肠黏膜和外周血单个核细胞中的表达及意义

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目的通过检测微小核糖核酸-155(microRNA-155,miR-155)在溃疡性结肠炎(UC)患者直肠黏膜和外周血单个核细胞(PBMC)中的表达,探讨miR-155在UC中的作用及意义。方法选择2016年3月至9月诊治的25例活动期UC患者(UC组)及同期15例结肠息肉患者(对照组),肠镜下观察患者肠道黏膜炎症表现,并行直肠黏膜活检(其中结肠息肉患者取其正常直肠黏膜)作病理学检查。实时荧光定量PCR(qRT-PCR)检测直肠黏膜中miR-155、白介素(IL)-17 mRNA、IL-6 mRNA及PBMC中miR-155的表达,直肠黏膜中miR-155与IL-17 mRNA、IL-6mRNA表达的关系采用Pearson相关性分析;免疫组织化学方法检测直肠黏膜中IL-17、IL-6蛋白的表达情况并进行表达评分,分析直肠黏膜及PBMC中miR-155的水平与患者临床特征的关系。结果 25例活动期UC患者,其直肠黏膜中miR-155相对表达量明显高于对照组(13.57±2.78 vs 1.02±0.05,P<0.01);PBMC中miR-155相对表达量亦明显高于对照组(23.68±4.23 vs 0.92±0.04,P<0.01);直肠黏膜中IL-17 mRNA(7.79±1.45 vs 1.20±0.05)及IL-6 mRNA(6.10±1.17 vs 1.02±0.03)相对表达量均高于对照组(P均<0.05)。相关性分析显示,直肠黏膜中miR-155与IL-17 mRNA、IL-6 mRNA的表达呈正相关(r=0.934,P<0.01;r=0.909,P<0.01)。活动期UC患者直肠黏膜免疫组化IL-17蛋白表达评分[(3.44±0.25)分vs(1.20±0.18)分]及IL-6蛋白[(3.12±0.28)分vs(0.80±0.17)分]高于对照组(P均<0.01)。相关分析显示,miR-155在活动期UC患者直肠黏膜及PBMC中的相对表达量,与患者疾病活动指数呈正相关(r=0.804,P<0.01;r=0.813,P<0.01);与患者年龄(r=0.067,P>0.05;r=0.006,P>0.05)及性别无关(r=0.151,P>0.05;r=0.202,P>0.05)。结论 miR-155可能参与了UC的发病,其机制可能与促进辅助性T细胞(Th)17分泌的致炎因子IL-17和IL-6的表达有关,可为UC患者病情活动性及严重程度的评价提供参考。 Objective To investigate the role of miR-155 in UC by detecting the expression of microRNA-155 (miR-155) in rectal mucosa and peripheral blood mononuclear cells (PBMCs) in patients with ulcerative colitis (UC) And meaning. Methods Twenty-five active UC patients (UC group) and 15 patients with colonic polyps from March to September in 2016 (control group) were enrolled in this study. Intestinal mucosal inflammation was observed under endoscopy and biopsy of rectal mucosa Colon polyps patients take their normal rectal mucosa) for pathological examination. The expression of miR-155, IL-17 mRNA and IL-6 mRNA and PBMC in rectal mucosa were detected by real-time quantitative PCR (qRT-PCR) Pearson correlation analysis was used to analyze the relationship between the expression of IL-6mRNA and IL-6mRNA. The expression of IL-17 and IL-6protein in rectal mucosa was detected by immunohistochemical method. Characteristics of the relationship. Results The relative expression of miR-155 in rectal mucosa of 25 active UC patients was significantly higher than that of the control group (13.57 ± 2.78 vs 1.02 ± 0.05, P <0.01). The relative expression of miR-155 in PBMC was also significantly higher than that of the control (23.68 ± 4.23 vs 0.92 ± 0.04, P <0.01). The relative expression of IL-17 mRNA (7.79 ± 1.45 vs 1.20 ± 0.05) and IL-6 mRNA in rectal mucosa (6.10 ± 1.17 vs 1.02 ± 0.03) In the control group (all P <0.05). Correlation analysis showed that there was a positive correlation between the expression of miR-155 and IL-17 mRNA and IL-6 mRNA in rectal mucosa (r = 0.934, P <0.01; r = 0.909, P <0.01). The expression of IL-17 protein in rectal mucosa of active UC patients [(3.44 ± 0.25) vs (1.20 ± 0.18) and IL-6 [3.12 ± 0.28 vs 0.80 ± 0.17] Higher than the control group (P <0.01). Correlation analysis showed that the relative expression level of miR-155 in rectal mucosa and PBMC of active UC patients was positively correlated with disease activity index (r = 0.804, P <0.01; r = 0.813, P <0.01) (r = 0.067, P> 0.05; r = 0.006, P> 0.05) and gender (r = 0.151, P> 0.05; r = 0.202, P> 0.05). Conclusion miR-155 may be involved in the pathogenesis of UC. Its mechanism may be related to the expression of IL-17 and IL-6, which are the proinflammatory cytokines that promote secretion of helper T cells (Th17), and may be used as a marker of disease activity and severity in patients with UC Provide a reference for the evaluation.
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