| 溃疡性结肠炎模型的构建及其炎症反应机制研究 |
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| 引用本文： | 王倩,田慧,刘靓靓,钟明,梅艳飞,张力.溃疡性结肠炎模型的构建及其炎症反应机制研究[J].河北北方学院学报(医学版),2014(5):15-23. |
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| 作者姓名： | 王倩 田慧 刘靓靓 钟明 梅艳飞 张力 |
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| 作者单位： | 河北北方学院,中国张家口075000 |
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| 基金项目： | 国家自然科学基金项目（No.81274005） |
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| 摘 要： | 目的：构建2,4,6-三硝基苯磺酸（2,4,6-trinitrobenzene sulfonic acid,TNBS）以及恶唑酮（oxazolone,OXZ）诱导的小鼠溃疡性结肠炎（ulcerative colitis,UC）模型。方法：120只昆明小鼠（）随机分为4组（n=30）。Ⅰ组、Ⅱ组参照Morris及Walter的方法制备小鼠TNBS模型：Ⅰ组（TNBS溶剂对照组）,50%乙醇0.1 m L灌肠;Ⅱ组（TNBS模型组）,0.6%TNBS溶液0.1 m L灌肠;两组灌肠给药一次后在d 1、d 2、d 3、d 5、d 7每组处死6只。Ⅲ组、Ⅳ组参照Heller方法制备小鼠OXZ模型：Ⅲ组（OXZ溶剂对照组）,皮肤涂抹100%乙醇0.1 m L,每天一次,连续2 d,d 7以50%乙醇0.1 m L灌肠;Ⅳ组（OXZ模型组）,皮肤涂抹1%OXZ溶液（100%乙醇溶解）0.1 m L每天一次,连续2 d（致敏）,d 7以0.5%OXZ（50%乙醇溶解）0.1 m L灌肠;两组灌肠给药一次后在d 1~d 5每天处死6只小鼠。观察Ⅰ~Ⅳ组小鼠疾病活动指数（disease activity index,DAI）、结肠组织大体损伤指数（colon macroscopic damage index,CMDI）和病理组织学评分（histopathological score,HPS）,并检测小鼠结肠组织中髓过氧化物酶（myeloperoxidase,MPO）、白细胞介素-4（interleukin-4,IL-4）、肿瘤坏死因子-α（tumor necrosis factor-α,TNF-α）的水平。结果：两种模型组小鼠DAI,CMDI和HPS均较对照组有明显改变;TNBS和OXZ诱导的结肠炎均可导致MPO明显上升,TNBS结肠炎TNF-α明显上升,OXZ结肠炎IL-4明显下降。结论：TNBS及OXZ均能诱导小鼠溃疡性结肠炎模型。两种模型各有特点,其中TNBS诱导的小鼠溃疡性结肠炎以辅助性T1（helper1,Th1）型炎症反应为主,OXZ诱导的小鼠溃疡性结肠炎以辅助性T2（helper2,Th2）型炎症反应为主。
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| 关 键 词： | 溃疡性结肠炎 2 4 6-三硝基苯磺酸(TNBS) 恶唑酮(OXZ) 白细胞介素-4(IL-4) 肿瘤坏死因子-α(TNF-α) |
Establishment of Model About Ulcerative Colitis and the Mechanism of Colitis-Related Inflammatory Responses |
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| WANG Qian,TIAN Hui,LIU Liang-jing,ZHONG Ming,MEI Yan-fei,ZHANG Li.Establishment of Model About Ulcerative Colitis and the Mechanism of Colitis-Related Inflammatory Responses[J].Journal of Hebei North University:Medical Edition,2014(5):15-23. |
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| Authors: | WANG Qian TIAN Hui LIU Liang-jing ZHONG Ming MEI Yan-fei ZHANG Li |
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| Institution: | (Hebei North University, Zhangjiakou, 075000, China) |
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| Abstract: | Objective：To establish 2,4,6-trinitrobenzene sulfonic acid （TNBS） and oxazolone （OXZ） induced murine models of ulcerative colitis （UC）. Methods：Totally 120 mice （♂） were randomly divided into four groups （n=30）. I , Ⅱ group referring to Morris and Walter TNBS model mice were prepared： I group （TNBS solvent control group）, 50% ethanol 0.1 mL enema; Ⅱ group （TNBS model group）, 0.6% TNBS solution 0.1 mL enema;after the two groups enema administered once, on d 1, d 2, d 3,d 5,d 7,6 mice in each group were sacrificed. Ill, IV group referring to Heller OXZ model mice were prepared： Ⅲ group （OXZ solvent control group）, skin smear 100% ethanol 0.1 mL,once a day for 2 d,d 7 with 50 percent ethanol 0.1 mL enema; IV group （OXZ model group）, skin applicator 1% OXZ solution （ 100% ethanol solution） 0.1 mL once a day for 2 d （sensitization）,d 7 with 0.5% OXZ （50% ethanol solution） 0.1 mL enema;after the two groups enema administered once,on d 1 to d 5 6 mice in each group were sacrificed. Observed mice disease activity index （DAI）,colon macroscopic damage index （CMDI） and histopathological score （HPS） of group I -IV, and detected mice colon tissue myeloperoxidase （MPO）,interleukin-4 （IL-4）,tumor necrosis factor-α （TNF-α） levels. Results：Both models mice DAI, CMDI and HPS, compared with control group, had significantly changed; TNBS-induced colitis and OXZ can lead to significantly increased MPO, TNBS colitis TNF-ct significantly increased, OXZ colitis significantly decreased IL-4. Conclusion ： TNBS and OXZ could induce mouse model of ulcerative colitis,TNBS-induced mouse ulcerative colitis with Thl-type inflammation dominated,OXZ ulcerative colitis in mice induced Th2- type inflammatory response with the main , and so, ulcerative colitis is a result that Thl and Th2 imbalance adjusted. |
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| Keywords: | ulcerative colitis 2 4 6-trinitrobenzene sulfonic acid （TNBS） oxazolone（OXZ） interleukin-4 （IL-4） tumor necrosis factor-α （TNF-α） |
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