脂多糖诱导的小鼠急性肺损伤模型的建立

Modeling of Acute Lung Injury in Mice Challenged with LPS

急性肺损伤是由创伤、感染、休克等诸多非心源性因素导致的一种急性、进行性呼吸障碍。该病的主要特点是出现顽固型低氧血症、促进呼吸频数升高、呼吸加重、呼吸困难、X线分析结果显示肺泡多出现弥漫性浸润等。本实验通过气管滴注脂多糖的方法建立急性肺损伤动物模型,通过HE染色观察肺组织病理学变化、测定肺组织湿干重比值(W/D)、试剂盒检测肺组织MPO活性变化及促炎性细胞因子的产生变化,以验证小鼠急性肺损伤模型是否建立成功。结果表明,脂多糖刺激显著破坏了肺脏组织结构、促进了大量炎性细胞浸润并伴有肺泡壁增厚。脂多糖可以显著提高肺湿干重比率(W/D),促进BALF中TNF-α、IL-1β和IL-6的表达,并提高肺组织的MPO活性。这些结果表明,我们成功利用脂多糖建立了小鼠急性肺损伤模型。

Acute lung injury（ALI）is an acute and progressive respiratory dysfunction,which is usually caused by trauma,infection,shock,and many other non-cardiac causes.The main features of the disease are stubborn hypoxemia,the breath frequency increases,heavy breathing,dysonea,X-ray analysis showed a diffuse infiltration of alveolar.Model of acute lung injury was established in mice by instilling weasand with LPS.The acute lung injury in mice was evaluated by H.E dyeing,lung tissue for wet dry weight ratio（W/D）,MPO activity and inflammatory cytokines were determined.The results showed that lung organization structure damage,inflammatory cells infiltration and alveolar walls thickness were significantly induced by LPS.These results suggested that model of acute lung injury were successfully established in mice by instilling weasand with LPS.