ICAM-1等细胞因子在大鼠肠缺血再灌注状态下的改变及其对肠屏障功能的影响

发布时间：2018-08-04 20:04

【摘要】：目的:探讨肠缺血再灌注造成应激状态下细胞因子的变化及其对大鼠肠粘膜屏障功能改变的影响以及它们之间的相关性。 方法:健康Wistar大白鼠60只,随机分为实验组、对照组和正常组,每组20只。实验组通过以显微手术用无损伤动脉夹夹闭肠系膜上动脉起始部,1小时后松夹恢复肠系膜上动脉血流制成肠缺血后再灌流模型,对照组只进行同样腹部手术操作但不夹闭肠系膜上动脉。正常组不手术。6小时后处死动物,3组同样取距回盲部15厘米处肠管1厘米,常规固定石蜡包埋,组织切片,通过普通HE染色观察肠粘膜组织细胞学形态;用免疫组织化学方法染色显示肠粘膜组织或细胞中白细胞介素-6、转化生长因子β-3、基质金属蛋白酶-7及细胞间黏附分子-1的表达情况;并用VIDAS图象分析系统进行半定量分析。 结果:普通HE染色结果显示光镜下,实验组空肠与对照组相比,可见肠壁变薄,绒毛短细,绒毛间距变宽,上皮细胞水肿明显,部分坏死脱落。免疫组织化学染色显示:实验组肠粘膜上皮细胞胞浆中白细胞介素-6、基质金属蛋白酶-7;肠组织血管内皮细胞、肠粘膜固有层和单核巨噬细胞中细胞间黏附分子-1表达较对照组增高;粘膜上皮细胞胞浆转化生长因子β-3表达较对照组增高,上述结果统计学比较差异有显著性(P0.01)。对照组结肠与正常组相比无明显差异。 结论:由于缺血再灌注造成应激时,肠粘膜上皮细胞内白细胞介素-6、转化生长因子β-3表达失衡导致上皮细胞内基质金属蛋白酶-7、细胞间黏附分子-1表达增高,肠粘膜萎缩及通透性增大,导致肠屏障功能损伤。
[Abstract]:Aim: to investigate the changes of cytokines and the relationship between cytokines and intestinal mucosal barrier function in rats induced by intestinal ischemia-reperfusion. Methods: 60 healthy Wistar rats were randomly divided into experimental group, control group and normal group with 20 rats in each group. In the experimental group, the blood flow of the superior mesenteric artery was restored after 1 hour of occlusion of the superior mesenteric artery by microsurgical clamping of the superior mesenteric artery, and the model of intestinal ischemia and reperfusion was established. The control group only performed the same abdominal operation without clipping the superior mesenteric artery. The animals in the normal group were killed after 6 hours of operation. The intestinal tubes of group 3 were also removed from the ileocecal part 15 cm from the ileocecal part. The intestinal mucosa was embedded in paraffin wax and sectioned. The histological morphology of intestinal mucosa was observed by HE staining. The expressions of interleukin-6, transforming growth factor 尾 -3, matrix metalloproteinase-7 and intercellular adhesion molecule-1 in intestinal mucosal tissues or cells were detected by immunohistochemical staining, and semi-quantitative analysis was performed by VIDAS image analysis system. Results: the results of HE staining showed that compared with the control group, the jejunum of the experimental group was thinner, the villi were shorter, the chorion spacing was wider, the epithelial cells were edema, and some of them were necrotic and shedding. Immunohistochemical staining showed that interleukin-6 and matrix metalloproteinase-7 in the cytoplasm of intestinal mucosal epithelial cells in the experimental group, vascular endothelial cells in intestinal tissue, The expression of intercellular adhesion molecule-1 in intestinal lamina propria and mononuclear macrophages was higher than that in control group, and the expression of TGF- 尾 -3 in mucosal epithelial cells was higher than that in control group (P0.01). There was no significant difference in colon between the control group and the normal group. Conclusion: during the stress induced by ischemia-reperfusion, the imbalance of interleukin-6 and transforming growth factor 尾 -3 in intestinal epithelial cells leads to the increase of matrix metalloproteinase-7 and the expression of intercellular adhesion molecule-1 in epithelial cells. Intestinal mucosal atrophy and increased permeability lead to injury of intestinal barrier function.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R363

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