首页> 中文期刊> 《中国实验动物学报》 >急性肺损伤大鼠肺组织TOLL样受体4及CD14mRNA的表达

急性肺损伤大鼠肺组织TOLL样受体4及CD14mRNA的表达

             

摘要

目的 探讨内毒素致急性肺损伤大鼠肺组织TOLL样受体4及CD14 mRNA表达的变化.方法 24只雄性Wistar大鼠随机分为2组:对照组、LPS模型组,每组再分为4 h和8 h两个亚组.尾静脉注射脂多糖(LPS)(10 mg/kg)建立大鼠急性肺损伤模型.检测大鼠动脉血气、肺体指数,实时荧光定量PCR测定肺组织TOLL样受体4及CD14 mRNA的表达,并观察肺组织病理变化.结果 与对照组相比,模型组4 h和8 h时大鼠肺组织中的TLR4及CD14 mRNA表达均显著增高(P<0.05或P<0.01).病理学观察显示,模型组大鼠肺组织出现出血及坏死.结论 内毒素致急性肺损伤的发病机制可能与TLR4及CD14 mRNA的表达升高有关.%Objective To investigate the changes of TLR4 and CD14 mRNA expression in the rats with acute lung injury (ALI) induced by lipopolysaccharide (LPS) . Methods Twenty-four male Wistar rats were randomly divided into two groups: normal control group and LPS model group. Each group had two subgroups, 4 hours and 8 hours after LPS injection. The ALI model was established by intravenous injection of LPS ( 10 mg/kg) through the tail vein. The arterial blood gas graph (ABGG) and lung-body index were analyzed. The expressions of TLR4 and CD14 mRNA were measured by real-time fluorescent polymerase chain reaction (PCR), while the histopathology of the lung injury was observed by light microscopy. Results Compared with the normal group, the expressions of TLR4 and CD14 mRNA in LPS model group were significantly increased at 4 hours and 8 hours (P < 0.05 or P < 0. 01 ). Light microscopic observation indicated that there were pulmonary hemorrhage and necrosis in the model group. Conclusion The increase of TLR4 and CD14 mRNA expressions may be involved in the pathogenetic mechanism of acute lung injury caused by lipopolysaccharide.

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