丙泊酚对呼吸机所致肺损伤大鼠的保护作用及机制

目的探索丙泊酚对呼吸机所致肺损伤(VILI)模型大鼠的保护作用,并分析其调控机制。方法利用大潮气量通气建立肺损伤模型,将30只SD大鼠随机分为假手术组、模型组和丙泊酚组,每组10只。检测大鼠肺组织湿/干重比(W/D)、大鼠肺组织形态学变化情况、大鼠肺组织中TNF-α和IL-6含量以及JAK、STAT3 mRNA和蛋白水平,并比较3组大鼠肺组织中SOD、MDA的含量。结果与假手术组相比,模型组W/D明显较高,肺组织病理学形态较差,肺组织中TNF-α和IL-6含量明显较高,JAK、STAT3 mRNA水平较高,p-JAK、p-STAT3蛋白水平较高,MDA的含量较高,而SOD的含量较低,以上差异均有统计学意义(P<0.05);与模型组相比,丙泊酚组W/D明显较低,肺组织形态学得到改善,肺组织中TNF-α和IL-6含量明显较低,JAK、STAT3 mRNA水平较低,p-JAK、p-STAT3蛋白水平较低,MDA的含量较低,SOD的含量较高,以上差异均有统计学意义(P<0.05)。结论丙泊酚对VILI模型大鼠具有减弱炎症反应的作用,其机制可能与抑制JAK/STAT3信号通路有关。

Protective effects and mechanism of propofol on the model of ventilator-induced lung injury rats

Objective To explore the protective effects and underlying mechanism of propofol on the model of ventilator-induced lung injury rats.Methods The model of lung injury was established by high tidal volume ventilation,and the 30 SD rats were randomly divided into the sham operation group,the model group and the propofol group,with 10 rats in each group.The wet/dry weight ratio(W/D)of rat lung tissue,the lung histomorphological changes of rats,the contents of TNF-αand IL-6,the levels of JAK,STAT3 mRNA and protein,and the contents of SOD and MDA in the lung tissues of the rats in the three groups were detected.Results After treatment for the model group,there were higher W/D value,poorer pathological histology of lung,higher contents of TNF-αand IL-6 in lung tissues,higher levels of JAK,STAT3 mRNA,higher p-JAK,p-STAT3 protein levels,higher SOD,and lower MDA,with statistically significant differences compared to those in the sham operation group(P<0.05).After treatment for the propofol group,there were lower W/D value,better pathological histology of lung,lower contents of TNF-αand IL-6 in lung tissues,lower levels of JAK,STAT3 mRNA,lower p-JAK,p-STAT3 protein levels,lower SOD,and higher MDA,with statistically significant differences compared to those in the model group(P<0.05).Conclusion Propofol can inhibit the inflammatory response in the model of ventilator-induced lung injury rats,and the underlying mechanism may be related to inhibiting JAK/STAT3 signaling pathway.