【作者】 陈朝辉；

【导师】 徐昆；

【作者基本信息】 重庆医科大学 ， 麻醉学， 2004， 硕士

【摘要】 目的:体外观察抑肽酶抑制中性粒细胞对TNFα活化的人脐静脉内皮细胞黏附和迁移，探讨其抑制体外循环术后全身性系统性炎症反应的机制。方法:采用Ficoll液提取高纯度的人中性粒细胞，使之与不同处理的人脐静脉内皮细胞黏附，计算黏附率。采用细胞培养小室测定中性粒细胞跨迁单层融合的人脐静脉内皮细胞的迁移率，采用免疫细胞化学法观察抑肽酶对TNFα活化的人脐静脉内皮细胞ICAM-1，β-catenin表达的改变。结果:1. TNFα未活化人脐静脉内皮细胞时，中性粒细胞和人脐静脉内皮细胞的黏附率为30.19%±3.23%,迁移率为16.63%±2.27%,活化后，黏附率上升到46.54%±3.59%,迁移率上升到41.70%±3.37%,抑肽酶预先作用并持续存在时，相同浓度的TNFα刺激相同时间，中性粒细胞和人脐静脉内皮细胞的黏附率为32.99%±3.43%,仅微弱增加，迁移率为27.48%±2.74%,增加幅度明显减少。2． 抑肽酶可抑制TNFα活化的人脐静脉内皮细胞ICAM-1的表达，可避免β-catenin的丢失。 <WP=7>结论：抑肽酶可抑制抑制中性粒细胞对TNFα活化的人脐静脉内皮细胞黏附和迁移，抑肽酶抑制体外循环术后全身性系统性炎症反应与抑肽酶抑制血管内皮细胞ICAM-1，β-catenin表达的改变有关。更多还原

【Abstract】 Objective: To study the anti-inflammatory mechanism of aprotinin in the prevention of systemic inflammation after cardiopulmonary bypass. Methods: We observed the adhesion between polymorphonuclear neutrophils(PMN) and human umbilicus vein endothelial cells in different conditions, and studied the neutrophils transmigration through cultured human umbilicus vein endothelial cells(ECV-304 ) in response to the chemoattractants: platelet-activating factor(PAF). Immunocytoche- mical staining was used to observe the changes in the expression of ICAM-1,β-catenin of the endothelial cells. Results: 1. The firm adhesion rate and transmigration rate increased from 30.19%±3.23% to 46.54%±3.59%,16.63%±2.27% to 41.70%±3.37%,respectly after TNFαstimulated ECV-304.But,when aprotinin existed,the firm adhesion rate and transmigration rate added up to only 32.99%±3.43%,27.48%±2.74%, respectly.The increasing extent downgrated obviously. <WP=9>2.Aprotinin could downgrade the expression of ICAM-1 of TNFα activating endothelial cells and prevent the loss of β-catenin of the cells,protect the adherens junctions of endothelials cells.Conclusions: Aprotinin exerted obvious effect on the firm adhesion and significantly inhibited neutrophils transmigration through cultured human umbilicus vein endothelial cells (ECV-304) in response to the chemoattractants: platelet-activating factor(PAF). Aprotinin inhibited the systemic inflammation after cardiopulmonary bypass,which may be relevant to the downgrated expression of ICAM-1 and the prevented loss of β-catenin through the use of aprotinin.更多还原