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The Effect Of Aprotinin On Polymorphonuclear Neutrophils (PMN) Adhesion And Transmigration Through TNFα Activated Human Umbilicus Vein Endothelial Cells In Vitro

Posted on:2005-03-06Degree:MasterType:Thesis
Country:ChinaCandidate:C H ChenFull Text:PDF
GTID:2144360122990107Subject:Anesthesia
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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. 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.
Keywords/Search Tags:aprotinin, cardiopulmonary bypass, systemic inflammation response, anti-inflammatory mechanism.
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