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鲁香凤,张书信,傅丽元,戴欣,孙浩.人溃疡性结肠炎与大鼠模型的组织病理学变化比较及机制探讨[J].中国实验动物学报,2018,26(5):597~602.
人溃疡性结肠炎与大鼠模型的组织病理学变化比较及机制探讨
Comparison of histopathological changes in large intestinal mucosa between human ulcerative colitis and a induced rat model by sodium dextran sulfate
投稿时间:2018-04-12  
DOI:10.3969/j. issn. 1005 - 4847. 2018. 05. 010
中文关键词:  溃疡性结肠炎  组织病理学变化  葡聚糖硫酸钠  病理机制
英文关键词:ulcerative colitis  histopathological changes  dextran sulfate sodium  pathological mechanisms
基金项目:
作者单位E-mail
鲁香凤 北京中医药大学东直门医院病理科,北京 100700 xiangfenglu@163. com 
张书信 北京中医药大学东直门医院肛肠科,北京 100700 13661027611@126. com 
傅丽元 北京中医药大学东直门医院肛肠科,北京 100700  
戴欣 北京中医药大学东直门医院病理科,北京 100700  
孙浩 北京中医药大学东直门医院病理科,北京 100700  
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中文摘要:
      目的 对葡聚糖硫酸钠(DSS)复制大鼠溃疡性结肠炎(UC)与人UC 大肠黏膜组织病理学变化进行比较,并探讨其机制?方法 SPF 级SD 雄性大鼠20 只,分为正常组和模型组(自由饮用5% DSS)各10 只,观察大鼠一般情况?大肠外观及黏膜组织病理学变化;选取我院9 例人UC 做对照?结果 DSS 模型与人UC 共同病变为大肠黏膜隐窝炎?隐窝脓肿?结构紊乱及萎缩?糜烂及溃疡等;不同之处为:DSS 模型早期病变始于固有膜下1/3 隐窝萎缩消失,逐渐发展至全层隐窝消失,间质以巨噬细胞为主,未见浆细胞,然后表面上皮变性坏死脱落?糜烂溃疡形成,多个血管腔内可见血栓,偶见机化,腺体不典型增生发生率低;而人UC 早期病变始于表面上皮及上1/3 隐窝急性炎,隐窝破坏萎缩与隐窝脓肿明显相关,均伴慢性肠炎基础病变及腺体不典型增生,偶见血栓伴/ 不伴机化?结论 二者的共同点为大肠黏膜隐窝干细胞损伤,不同点为DSS 首先损伤隐窝干细胞,炎症是继发,而人UC 则相反,如采用该模型研究药物疗效及其机制需辨证分析其结果?
英文摘要:
      Objective To compare the histopathological changes of large intestinal mucosa between a rat ulcerative colitis (UC) model induced by dextran sulfate sodium (DSS) and human UC, and examine the pathological mechanisms. Methods Twenty healthy Sprague Dawley male rats (specific?pathogen?free grade)were divided into normal control and model (free access to 5% DSS solution) groups (n =10 per group). The general condition, appearance of the large intestine, and histopathological changes of the mucosa in rats were compared with nine cases of human UC admitted in our hospital. Results The most common lesions involved large intestinal cryptitis, crypt abscesses, crypt atrophy and structural disorder, and erosion and ulcer formation in the rat and human UC cases. In the majority of rats, early lesions showed atrophy of ~1/3 of crypts in the inferior lamina propria, which gradually developed to the entire layer. Interstitial inflammation predominantly involved macrophages, with no plasma cells. The surface epithelia then degenerated, with necrosis and shedding, and formation of a mucosal ulcer, followed by multiple intravascular thrombosis, individual thrombus organization, and occasional glandular dysplasia. By contrast, early stage human UC typically involved acute inflammation of surface epithelia and the upper 1/3 of crypts, while glandular destruction and atrophy were associated with crypt abscesses. All of the human cases were accompanied by basic pathological changes involving chronic enteritis and atypical gland hyperplasia, and occasional thrombosis with/ without organization. Conclusions The common pathogenesis of UC in human ulcerative colitis and DSS?induced rat UC involves injury of large intestinal crypt stem cells. However, DSS?treated rats showed initial lower 1/3 crypt damage expanding into whole crypt destruction, with secondary inflammation, while human UC showed the opposite pattern. These differences should be considered when using this model to study the efficacy and mechanism of drugs for treatment of Ulcerative colitis.
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