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目的探讨急性胆道感染时大鼠肝组织中脂多糖(lipopolysaccharide,LPS)受体CD14的表达及其对细胞因子分泌的影响。方法通过结扎Wistar大鼠胆总管,在胆总管内注入大肠杆菌O111∶B4,复制急性胆道感染动物模型。于术后0、3、6、12、24 h分别检测肝组织中CD14蛋白和mRNA表达水平,血浆内毒素、TNF-α和IL-6的含量、枯否细胞(kupffer cells,KCs)吞噬活性,电镜观察KCs超微结构的变化。结果在急性胆道感染时随着感染时间延长,血浆内毒素浓度逐渐升高,KCs呈现激活的改变,血浆TNF-α、IL-6含量明显增加,而此时肝组织中CD14的表达也显著增加。结论急性胆道感染时肝组织中CD14的表达进行性增强,KCs激活,释放的细胞因子也逐渐增多,这可能是急性胆道感染时KCs致炎作用增强的重要机制之一。
Objective To investigate the expression of lipopolysaccharide (LPS) receptor CD14 in rat liver tissue and its effect on the secretion of cytokines in acute biliary tract infection. Methods Wistar rat common bile duct was ligated and E.coli O111: B4 was injected into the common bile duct to replicate the animal model of acute biliary tract infection. The levels of CD14 protein and mRNA in liver tissue were measured at 0, 3, 6, 12 and 24 h after operation. The levels of endotoxin, TNF-α and IL-6, phagocytic activity of Kupffer cells The changes of ultrastructure of KCs were observed by electron microscope. Results In acute biliary tract infection, with the prolongation of infection time, plasma endotoxin concentration gradually increased, KCs showed activation changes, plasma TNF-α, IL-6 levels increased significantly, while the expression of CD14 in liver tissue was also significantly increased . Conclusions The expression of CD14 in liver tissue is progressively increased in acute biliary tract infection. The activation of KCs and the release of cytokines also gradually increase, which may be one of the important mechanisms of KCs enhanced inflammation in acute biliary tract infection.