溃疡性结肠炎结肠黏膜脱氧核糖核酸甲基转移酶3a表达及作用研究
The expression and role of DNA methyltrsansferase 3a in colonic mucosa of patients with ulcerative colitis
摘要目的 探讨溃疡性结肠炎(UC)患者结肠黏膜固有层内单个核细胞中脱氧核糖核酸甲基转移酶3a(DNMT3a)与白细胞介素-4(IL-4)、γ-干扰素(IFN-γ)表达的相关性.方法 选取2009年11月至2010年3月天津医科大学总医院60例结肠内镜活检标本,其中活动期UC和正常对照组各30例.应用免疫组织化学染色法(SABC法)检测各组结肠黏膜固有层内单个核细胞中DNMT3a、IL-4、IFN-γ的表达,分析三者与不同程度结肠炎性反应的关系.结果 UC组结肠黏膜固有层内单个核细胞中DNMT3a、IL-4、IFN-γ的表达阳性率均高于正常对照组,差异有统计学意义(x2分别=16.596、42.857和6.667,P值分别=0.000、0.000和0.024).三者在重度炎性反应组中的表达强度均高于轻中度炎性反应组,且其表达强度随疾病活动度加重而升高.UC组IL-4、IFN-γ表达与DNMT3a表达均呈正相关(r值分别=0.460和0.559,P值分别=0.010和0.001).结论 UC结肠黏膜中DNMT3a、IL-4、IFN-γ表达与结肠炎性反应程度相关,DNA甲基化可能参与UC发病过程中Th1/Th2免疫平衡的调节.
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abstractsObjective To explore the association between DNA methyltrsansferase 3a (DNMT3a) expression and interleukin-4 (IL-4),interferon-gamma (IFN-γ) in mononuclear cells of colonic laminapropriamucosae in ulcerative colitis (UC) patients.Methods From November 2009 to March 2010,sixty colonic mucosa biopsy specimens through colon scopy were collected,specimens of active UC or normal controls were 30 in each group.The expression of DNMT3a,IL-4,and IFN-γ was detected with immunohistochemical method (SABC) in mononuclear cells of colonic laminapropriamucosae,and their relation with different degrees of colonic inflammatory response was analyzed.Results The positive expression rate of DNMT3a,IL-4,IFN-γ in mononuclear cells of colonic laminapropriamucosae in active UC group was significant higher than that in control group and there were statistically significant differences (x2 =16.596,P=0.000;x2 =42.857,P=0.000;x2 =6.667,P=0.024;).The expression of them was higher in sever inflammatory response than that in mild inflammatory response,and its expression intensity increased as inflammatory activity became more severe.There was positive correlation between IL-4,IFN-γ and DNMT3 expression in UC group (r=0.46,P=0.01 ;r=0.559,P=0.001).Conclusions The expression of DNMT3a,IL-4 and IFN-γ is associated with the degree of colonic inflammatory response.DNA methylation maybe involved in Th1/Th2 immune balance regulation in UC pathogenesis.
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