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Effect of tight junction protein of intestinal epithelium and permeability of colonic mucosa in pathogenesis of injured colonic barrier during chronic recovery stage of rats with inflammatory bowel disease

机译:炎症性肠病慢性恢复期肠上皮紧密连接蛋白和结肠黏膜通透性在受损结肠屏障发病机制中的作用

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摘要

Objective: To discuss the changes in the tight junction protein of intestinal epithelium and permeability of colonic mucosa and its possible mechanism by building the rat mode of inflammatory bowel disease at the chronic recovery stage. Methods: A total of 36 SD rats were divided into the model group and control one according to the random number table, with 18 rats in each group. Rats in the model group were given the 3% dextran sulfate sodium solution by the way of drinking for 7 d to build the rat model of inflammatory bowel disease, while rats in the control group were given free drinking of water. Six rats were executed at day 7, 14 and 21 respectively. The colonic tissues were collected from rats to observe the pathological changes of colonic mucosa. The activity of myeloperoxidase was detected and the white blood count was performed for rats in each group. The Ussing chamber technique was employed to detect the transepithelial electrical resistance (TER) and short-circuit current (SC) of colonic mucosa of rats in different time intervals; the quantum dots labeling technique was employed to detect the expression level of claudin-1 and claudin-2 in the colonic tissues. Results: After the successful modeling, the weight of rats in the model group was significantly reduced, while the disease activity index score was increased. The weight was at the lowest level at day 14 and then it began to increase afterwards. The disease activity index score was at the highest level at day 12 and then it began to decrease gradually. The activity of myeloperoxidase and WBC for rats in the model group all reached the peak value at day 14 and then decreased gradually. There was no significant difference in the changes of TER and SC in different time intervals for rats in the control group (P>0.05). TER of model group was at the lowest level at day 14 and then increased gradually;SC was at the highest level at day 14 and then decreased gradually. TER of model group at day 7, 14 and 21 was significantly lower than that of control group, while SC of model group was significantly higher than that of control group (P<0.05). There was no significant difference in the change of mean fluorescence intensity of claudin-1 and claudin-2 in different time intervals for rats in the control group (P>0.05). The claudin-1 and claudin-2 for rats in the model group reached the highest level at day 14 and then decreased gradually. The claudin-1 and claudin-2 of model group at day 7, 14 and 21 was significantly higher than that of control group (P<0.05). Conclusions:After the acute stage, the inflammatory bowel disease is then in the chronic recovery stage; the increased permeability of colonic mucosa and increased expression of tight junction protein of intestinal epithelium are closely related to the pathogenesis and development of disease. The tight junction protein plays a key role in the pathogenesis of injured colonic barrier of inflammatory bowel disease.
机译:目的:通过建立慢性恢复期大鼠炎症性肠病的模式,探讨肠道上皮紧密连接蛋白的变化和结肠黏膜通透性的变化及其可能的机制。方法:将36只SD大鼠按照随机数字表分为模型组和对照组,每组18只。模型组大鼠饮水7 d,给予3%右旋糖酐硫酸钠溶液,建立炎性肠病模型,对照组大鼠自由饮水。分别在第7、14和21天处死6只大鼠。从大鼠收集结肠组织,观察结肠粘膜的病理变化。检测髓过氧化物酶的活性,并在每组中对大鼠进行白血球计数。采用Ussing chamber技术检测不同时间间隔大鼠结肠黏膜的跨上皮电阻(TER)和短路电流(SC)。采用量子点标记技术检测结肠组织中claudin-1和claudin-2的表达水平。结果:成功建立模型后,模型组大鼠体重明显减轻,疾病活动性指数评分增加。体重在第14天处于最低水平,然后开始增加。疾病活动指数评分在第12天达到最高水平,然后开始逐渐下降。模型组大鼠髓过氧化物酶和白细胞的活性均在第14天达到峰值,然后逐渐下降。对照组大鼠在不同时间间隔的TER和SC变化无明显差异(P> 0.05)。模型组的TER在第14天最低,然后逐渐升高; SC在第14天最高,然后逐渐降低。模型组在第7、14和21天的TER显着低于对照组,而模型组的SC显着高于对照组(P <0.05)。对照组大鼠不同时间间隔claudin-1和claudin-2平均荧光强度变化无明显差异(P> 0.05)。模型组大鼠的claudin-1和claudin-2在第14天达到最高水平,然后逐渐下降。模型组在第7、14和21天的claudin-1和claudin-2明显高于对照组(P <0.05)。结论:急性期后,炎症性肠病进入慢性恢复期。结肠粘膜通透性增加和肠上皮紧密连接蛋白表达增加与疾病的发生发展密切相关。紧密连接蛋白在炎性肠病的受损结肠屏障的发病机理中起关键作用。

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  • 来源
    《亚太热带医药杂志(英文版)》 |2016年第2期|143-147|共5页
  • 作者单位

    Section B, Department of Gastroenterology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang, Hubei 441000, China;

    Section B, Department of Gastroenterology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang, Hubei 441000, China;

    Section B, Department of Gastroenterology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang, Hubei 441000, China;

    Section B, Department of Gastroenterology, Xiangyang Hospital Affiliated to Hubei University of Medicine, Xiangyang, Hubei 441000, China;

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