蛇床子素对脂多糖诱导的小鼠急性肺损伤的保护作用及机制研究

摘要

目的：探讨蛇床子素( Osthole,Ost)对脂多糖( Lipopolysaccharide,LPS)诱导的急性肺损伤的作用及其机制。方法45只雄性C57小鼠随机分为3组：正常对照组(对照组),LPS组,Ost+LPS组( Ost组),每组15只。各组小鼠于腹腔注射LPS或生理盐水(50 mg/kg)6 h后,测定PaO2、PaCO2、pH,IL-6、IL-1β、TNF-α表达,JAK2、STAT3、p-JAK2和p-STAT3蛋白表达量,观察肺组织病理变化和湿干比( W/D)。结果与LPS组比较,Ost组PaCO2、W/D,IL-6、IL-1β和TNF-α表达,p-JAK2和p-STAT3蛋白表达量和肺组织病理改变均明显降低,但PaO2和pH增高,而JAK2和STAT3表达无明显变化。结论 Ost预处理可通过抑制JAK2/STAT3信号通路激活而减轻LPS诱导的急性肺损伤。%Objective To investigate the protective effect of osthole ( Ost) on LPS-induced acute lung injury in mice and its mechanism. Methods 45 male C57 mice were randomly divided into three groups:control group ( con-trol),LPS group(LPS),andosthole+LPS group (Ost). PaO2,PaCO2 and pH,the expression of pro-inflammatory cy-tokines IL-6,IL-1β and TNF-α in lung tissue and serum,the protein level of JAK2,STAT3,p-JAK2 and p-STAT3 in lung tissue, the pathological change and Wet/Dry after 6 h of LPS or saline injection of the mice were exam-ined. Results Compared with LPS group,PaCO2 and Wet/Dry,the expression of pro-inflammatory cytokines IL-6,IL-1β and TNF-αin lung tissue and serum,the protein level of JAK2,STAT3,p-JAK2 and p-STAT3 in lung tissue and the pathological changes in lung tissues significantly decreased,and PaCO2 ,pH and Wet/Dry increased. Moreover,the pro-tein expression level of JAK2 and STAT3 had no significant difference. Conclusion Ost pretreatment can protect mice against LPS-induced acute liver injury by suppressing JAK2/STAT3 signal pathway.