Expression of MAdCAM-1 and nuclear factor kappa B and the intervention effect of nitric oxide donor in oxazolone-induced colitis
- Author:
- No author available
- Journal Title:
- WORLD CHINESE JOURNAL OF DIGESTOLOGY
- Issue:
- 6
- DOI:
- 10.3969/j.issn.1009-3079.2008.06.005
- Key Word:
- 恶唑酮;MAdCAM-1;核因子-κB;一氧化氮;溃疡性结肠炎
Abstract： 目的:探讨MAdCAM-1在恶唑酮结肠炎中的表达及一氧化氮供体DETA NONOate和GTN 对恶唑酮结肠炎的干预作用.方法:32只C57BL/6小鼠随机分为正常对照组(A)、恶唑酮结肠炎组(B)、GTN干预组(C)和DETA NONOate干预组(D).除正常对照组外,其余3组均建立小鼠恶唑酮结肠炎模型,两个一氧化氮供体干预后处死小鼠.评价DAI、大体评分和组织学评分;免疫组织化学法检测MAdCAM-1及NF-κB;硝酸还原酶法测定血清中NO含量:测定结肠组织MPO活性.结果:B组小鼠DAI评分自灌肠之日起逐渐增高,而D组则变化不明显.B组小鼠大体评分、组织学评分、NF-κB的表达、MAdCAM-1的表达、MPO活性(3.13±0.84,20.31±2.63,30.29±8.68,17.60±6.53,3.83±0.60)均分别高于A组(0.38±0.52,0.88±0.83,7.38±2.29,4.08±1.30,1.75±0.25,P＜0.01)和D组(1.38±0.52,11.13±1.48,12.60±3.54,8.42±2.16,2.76±0.48,P＜0.01),而C组则与B组相近.B组小鼠血清NO浓度高于A组(54.51±22.28vs 32.17±14.88,P＜0.05),而低于D组和C组(54.51±22.28 vs 88.53±24.77,80.12±19.79,均P＜0.05).B组MAdCAM-1的表达与组织学评分、MPO活性、NF-κB P65 IA值呈正相关(r=0.786,r=0.833,r=0.833,P＜0.05).结论:小鼠恶唑酮结肠炎中结肠固有层MAdCAM-1的表达增加,DETA NONOate可能是治疗溃疡性结肠炎的有价值药物.
- [1]韩英,村田有志,伊东重豪,等.长期应用尼古丁对恶唑酮诱导的实验性小鼠肠炎模型的影响及其机制探讨[J].2001,(8).
- [2]Gironella M,Iovanna J,Sans M,etc.Nitric oxide supplementation ameliorates dextran sulfate sodium-induced colitis in mice.[J].2002,82(5).
- [3]Jennings MH,Elrod JW,Joh T,etc.MAdCAM-1 Expression and Regulation in Murine Colonic Endothelial Cells In Vitro.[J].2005,11(3).
- [4]T, Oshima,P, Jordan,M B, Grisham,etc.TNF-alpha induced endothelial MAdCAM-1 expression is regulated by exogenous, not endogenous nitric oxide.[J].2001,1.
- [5]Isao Okayasu,Shigeru Hatakeyama,Masahiro Yamada,etc.A novel method in the induction of reliable experimental acute and chronic ulcerative colitis in mice[J].1990,98(3).
- [6]Ekstrom GM.Oxazolone-induced colitis in rats: effects of budesonide, cyclosporin A, and 5-aminosalicylic acid.[J].1998,33(2).
- [7]Sahin T,Hulagu S,Aygun C,etc.Endothelial dysfunction in patients with ulcerative colitis.[J].2006,12(3).
- [8]Hinoda Y,Goto A,Shinomura Y,etc.Antisense therapy of MAdCAM-1 for trinitrobenzenesulfonic acid-induced murine colitis.[J].2006,12(8).
- [9]Pavlick KP,Verma SK,Jordan P,etc.Regulation and distribution of MAdCAM-1 in endothelial cells in vitro.[J].2001,281(4).
- [10]K, Teramoto,S, Miura,Y, Tsuzuki,etc.Increased lymphocyte trafficking to colonic microvessels is dependent on MAdCAM-1 and C-C chemokine mLARC/CCL20 in DSS-induced mice colitis.[J].2005,139(3).
- [11]J K, MacDonald,J W D, McDonald.Natalizumab for induction of remission in Crohn's disease.[J].2007,(1).
- [12]Arihiro S,Ohtani H,Suzuki M,etc.Differential expression of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) in ulcerative colitis and Crohn's disease.[J].2002,52(5).
- [13]Nieuwenhuis EE,Blumberg RS,Strober W,etc.Oxazolone Colitis, a Th2 Colitis Model Resembling Ulcerative Colitis, Is Mediated by IL-13-Producing NK-T Cells.[J].2002,17(5).
- [14]M, Briskin,D, Winsor-Hines,A, Shyjan,etc.Human mucosal addressin cell adhesion molecule-1 is preferentially expressed in intestinal tract and associated lymphoid tissue.[J].1997,151.