溃疡性结肠炎肠黏膜中Act1、IL-17、NF-<em>κ</em>Bp65的表达及意义-东南大学学报医学版

溃疡性结肠炎肠黏膜中Act1、IL-17、NF-κBp65的表达及意义

单位：溧水县人民医院消化内科, 江苏溧水 211200

分类号：R574.62

出版年·卷·期（页码）：2013·32·第五期（599-602）

摘要：

目的:探讨溃疡性结肠炎(UC)肠黏膜组织中细胞质衔接蛋白(Act1)、核转录因子-κB p65(NF-κB p65)、白介素17(IL-17)的表达及三者在UC发病机制中的作用。方法:30例UC活动期病例为UC组,按肠黏膜病理学分级将UC组进一步分为Ⅰ级组、Ⅱ级组、Ⅲ级组。将健康体检者或结肠单发息肉切除术后复查肠镜结果正常者(30例)设为正常对照组。各组结肠黏膜中Act1、NF-κB p65、IL-17的表达水平采用免疫组化SP法检测,组间比较采用单因素方差分析, UC组Act1、NF-κB p65与IL-17表达水平的相关关系采用Pearson等级相关分析。结果:UC组结肠黏膜表面上皮细胞和固有层Act1、NF-κB p65、IL-17表达均呈阳性,而且表达比正常对照组显著增强(P<0.05); UC各亚组之间表达强度依次为Ⅲ级>Ⅱ级>Ⅰ级,差异有统计学意义(P<0.05);肠黏膜中Act1、NF-κB p65与IL-17的表达均呈正相关关系。结论:UC肠黏膜中Act1、IL-17、NF-κB p65的表达均上调,并随UC病理分级的升高而表达增强。

Objective: To investigate adaptor protein(Act1),nuclear factor-κB (NF-κB p65 p65),interleu-kin 17 (IL-17) expression in the mucosa of ulcerative colitis (UC) and it's roles in the pathogenesis of UC.Methods: Thirty cases of UC active cases were included as UC group,they were divided into UC pathological grade Ⅰ,Ⅱ,Ⅲ group according to the intestinal mucosa pathological grade.Thirty subjects of health or the single colon polypectomy who's review were normal as a normal control group.The expression of Act1,NF-κB p65,IL-17 in colonic mucosa were detected by immunohistochemical SP method.Groups were compared using one-way ANOVA.The correlation between the expression of Act1,NF-κB p65,IL-17 and intestinal mucosa pathological grading were tested by Pearson rank correlation analysis.Results: In UC group,the expression of Act1,NF-κB p65,IL-17 in colonic mucosal surface epithelium and lamina propria were positive and significantly higher than those of the normal control group (P<0.05); In UC subgroup,expression level was grade Ⅲ>gradeⅡ>gradeⅠ,the difference was statistically significant (P<0.05).Expression of Act1,NF-κB p65 and IL-17 in intestinal mucosa showed a positive correlation.Conclusion: The expression of Act1,NF-κB p65,IL-17 of UC in the intestinal mucosa are significantly up-regulated,and increased with the rise of the the UC pathological grade.

参考文献：

[1] 王龙,向永胜,蒋锐,等.美沙拉嗪联合昆明海棠对溃疡性结肠炎临床疗效观察[J].现代医学,2011,39(1):79-81.
[2] 张苏闽,吴崑岚,丁义江,等.气药灌肠治疗溃疡性结肠炎的临床研究(附60例资料分析)[J].东南大学学报:医学版,2002,21(4):310-312.
[3] TRUELOVE S C,WITTE L J.Cortisone in ulcerative colitis.Final report on a therapeutic trial[J].Br Med J,1955,2(4847):1041-1048.
[4] SCHROEDER K W,TREMAINE W J,HSTRUP D M.Coated oral 5-aminosalicylic acid therapy for mildly to moderately active ulceractive colitis.A randomized study[J].N Engl J Med,1987,317:1625-1629.
[5] CHOW D K,LEONG R W,TSOI K K,et al.Long-term follow-up of ulcerative colitis in the Chinese population[J].Am J Gastroenterol,2009,104(3):647-654.
[6] DAVID Q S,STEPHAN R T.Immunopathogenesis of inflammatory bowel disease[J].World J Gastroenterol,2008,14(3):390-400.
[7] SHIMAMOTO M,UENO Y,TANAKA S,et al.Selective decrease in colonic CD56(+)T and CD161(+)T cells in the inflamed mucosa of patients with ulcerative colitis[J].World J Gastroenterol,2007,13(45):5995-6002.
[8] ANDRESEN L,JORGENSEN V L,PERNER A,et al.Activation of nuclear factor kappaB in colonic mucosa from patients with collagenous and ulcerative colitis[J].Gut,2005,54:503-509.
[9] NARENDER N,RATNA P,SHAILENDRA G,et al.T-bet is essential for the progression of experimental autoimmune encephalomyelitis[J].Immunology,2006,118(3):384-391.
[10] STASI R,Del POETA G,STIPA E,et al.Response to B-cell depleting therapy with rituximab reverts the abnormalities of T-cell subsets in patients with idiopathic thrombocytopenic purpura[J].Blood,2007,110(8):2824-2930.
[11] FUJINO S,ANDOH A,BAMBA S,et al.Increased expression of interleukin-17 in inflammatory bowel disease[J].Gut,2003,52(10):65-70.
[12] SEIDERER J,ELBEN I,DIEGELMANN J,et al.Role of the novel Th17 cytokine IL-17F in inflammatory bowel disease(IBD):upregulated colonic IL-17F expression in active Crohn's disease and analysis of the IL17Fp.His161 Arg polymorphism in IBD[J].Inflamm Boel Dis,2008,14(8):427-445.
[13] LINDEN A.A role for the cytoplasmic sdaptor protein Act1 in mediating IL-17 signaling[J].Sci STKE,2007,398(4):1-47.
[14] QIAN Y,QIAN C,HARTUPEE J,et al.The adaptor Act1 is required for interleukin 17-dependent signaling associated with autoimmune and inflammatory disease[J].Nat Immunol,2007,8(3):247-256.
[15] CHANG S H,PARK H,DONG C,et al.Actl adaptor protein is an immediate and essential signaling component of interleukin-17 receptor[J].J Biol Chem,2006,281(47):35603-35607.
[16] LI X,COMMANE M,NIE H,et al.Act1,an NF-kappaB-activating protein[J].Proc Natl Acad Sci,2000,97(19):10489-10493.
[17] KANAMORI M,KAI C,HAYASHIZAKI Y,et al.NF-kappaB actiator Act1 associates with IL-1/Toll pathway adaptor molecule TRAF6[J].FEBS Lett,2002,532(2),241-246.

服务与反馈：

【文章下载】【发表评论】【查看评论】【加入收藏】

提示：您还未登录，请登录！点此登录