乌司他丁对大鼠内毒素性急性肺损伤保护作用机制的研究

The Protective Effects of Ulinastatin on Lipopolysaccharide-induced Acute Lung Injury in Rats and Its Mechanisms

目的:研究乌司他丁(UT I)对大鼠内毒素性急性肺损伤(AL I)保护作用机制。方法:采用大鼠内毒素AL I模型,分别观察生理盐水对照组(N S组)、内毒素组(LPS组)、乌司他丁治疗组(UT I组)于LPS滴注4 h后动脉血气,血浆IL-8、M DA含量及测定肺湿/干重比。结果:LPS组、UT I组分别与N S组比较,其血浆IL-8、M DA、PaCO2以及肺湿/干重比都明显升高,PaO2明显降低且UT I组各观察指标值的变化小于LPS组,差异具有显著性。结论:乌司他丁对大鼠内毒素性急性肺损伤具有保护作用,机制可能与减少炎性介质与氧自由基的释放,抑制酶联反应有关。

Objective： To investigate the effects of urinastatin on lipopolysaccharide-induced acute lung injury in rats and its mechanisms. Methods： Thirty Wistar rats were divided randomly into saline control （NS group）, lipopolysaecharide group （LPS group）, urinastatin for treatment group （UTI group）. Models of endotoxin induced ALI were used to observe the indexes of lung wet/dry weight. Arterial blood was drawn for blood gas analysis. Interleukin-8 （IL-8） and Malonaldehyde Acetal （MDA） were assessed 4 hours after the lipopolysaccharide injection. Results： Compared with the NS group, the W/D, the content of MDA and IL-8 were significantly increased （P〈0.01） and there was a significant decrease in the level of arterial bicarbonate and partial pressure of oxygen in the LPS group （P〈0.01）; But in urinastatin for treatment group, these indexes of lung injury were significantly lower than those in the group of LPS （P〈0.05）. Conclusion; The high-expression of MDA and IL-8 should play important roles in lipopolysaccharide-induced acute lung injury. Urinastatin could protect lipopolysaccharide-induced acute lung injury by inhibiting the lung inflammatory injury.