【摘要】：目的:探討腸缺血再灌注造成應(yīng)激狀態(tài)下細(xì)胞因子的變化及其對(duì)大鼠腸粘膜屏障功能改變的影響以及它們之間的相關(guān)性。 方法:健康Wistar大白鼠60只,隨機(jī)分為實(shí)驗(yàn)組、對(duì)照組和正常組,每組20只。實(shí)驗(yàn)組通過(guò)以顯微手術(shù)用無(wú)損傷動(dòng)脈夾夾閉腸系膜上動(dòng)脈起始部,1小時(shí)后松夾恢復(fù)腸系膜上動(dòng)脈血流制成腸缺血后再灌流模型,對(duì)照組只進(jìn)行同樣腹部手術(shù)操作但不夾閉腸系膜上動(dòng)脈。正常組不手術(shù)。6小時(shí)后處死動(dòng)物,3組同樣取距回盲部15厘米處腸管1厘米,常規(guī)固定石蠟包埋,組織切片,通過(guò)普通HE染色觀察腸粘膜組織細(xì)胞學(xué)形態(tài);用免疫組織化學(xué)方法染色顯示腸粘膜組織或細(xì)胞中白細(xì)胞介素-6、轉(zhuǎn)化生長(zhǎng)因子β-3、基質(zhì)金屬蛋白酶-7及細(xì)胞間黏附分子-1的表達(dá)情況;并用VIDAS圖象分析系統(tǒng)進(jìn)行半定量分析。 結(jié)果:普通HE染色結(jié)果顯示光鏡下,實(shí)驗(yàn)組空腸與對(duì)照組相比,可見(jiàn)腸壁變薄,絨毛短細(xì),絨毛間距變寬,上皮細(xì)胞水腫明顯,部分壞死脫落。免疫組織化學(xué)染色顯示:實(shí)驗(yàn)組腸粘膜上皮細(xì)胞胞漿中白細(xì)胞介素-6、基質(zhì)金屬蛋白酶-7;腸組織血管內(nèi)皮細(xì)胞、腸粘膜固有層和單核巨噬細(xì)胞中細(xì)胞間黏附分子-1表達(dá)較對(duì)照組增高;粘膜上皮細(xì)胞胞漿轉(zhuǎn)化生長(zhǎng)因子β-3表達(dá)較對(duì)照組增高,上述結(jié)果統(tǒng)計(jì)學(xué)比較差異有顯著性(P0.01)。對(duì)照組結(jié)腸與正常組相比無(wú)明顯差異。 結(jié)論:由于缺血再灌注造成應(yīng)激時(shí),腸粘膜上皮細(xì)胞內(nèi)白細(xì)胞介素-6、轉(zhuǎn)化生長(zhǎng)因子β-3表達(dá)失衡導(dǎo)致上皮細(xì)胞內(nèi)基質(zhì)金屬蛋白酶-7、細(xì)胞間黏附分子-1表達(dá)增高,腸粘膜萎縮及通透性增大,導(dǎo)致腸屏障功能損傷。
[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.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類(lèi)號(hào)】：R363

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