中文摘要：

目的：探讨凉膈散对内毒素（LPS）诱导急性肺损伤（ALI）大鼠信号转导与转录激活子3（STAT3）和磷酸化STAT3蛋白表达的影响。方法：SPF级健康雌性Wistar大鼠156只,随机分为对照组、LPS组、LPS＋3个不同剂量凉膈散组、LPS＋地塞米松组。LPS造模动物,又分为注射LPS后1、2、4、8、16h不同时相处死组,每组6只。各组大鼠在给生理盐水或LPS后相应的时间处死、取材,用WesternBlot法观察大鼠肺组织STAT3、P-STAT3含量的动态变化。结果：与对照组比较,LPS组大鼠尾ivLPS后,肺组织内STAT3、P-STAT3蛋白表达明显增强,其表达分别在1h、2h后达到峰值,随后逐渐下降。与LPS组相比较,凉膈散各剂量组与地塞米松干预组能显著抑制肺组织内STAT3、P-STAT3的表达。结论：内毒素致急性肺损伤时出现肺组织STAT3、P-STAT3异常表达,凉膈散可以抑制其异常表达,而发挥对内毒素ALI的保护作用。

英文摘要：

Objective：To explore the effect of Lianggesan on STAT3 and P-STAT3 protein expression in rats lung during acute lung injury（ALI） induced by lipopolysaccharide.Methods：156 SPF-class health female Wistar rats were randomly divided into control group,LPS group,LPS＋3different doses（7.5,15,30 g crude drug/kg） Langgesan group,LPS ＋ dexamethasone group.LPS model animals were divided into 1,2,4,8,16 h groups after LPS injection,and six in each group.Putting to death and drawing rats in each group at the corresponding time after giving the saline or LPS,and then to determine the dynamic content changes of STAT3 and P-STAT3 in rats lung tissue by Western Blot.Results：the STAT3 and P-STAT3 in lung tissue of rats only expressed slightly in the control group.Compared with the control group,STAT3 protein expression of LPS group markedly enhanced in the 1h time（P0.01）,and reaching the maximal level,then decreased gradually;whereas the P-STAT3 protein expression reached the highest level at the 2h time（P0.01）,and also followed by a gradual decline.Compared with the LPS group,all Lianggesan groups and dexamethasone intervention group presented a significant inhibition to the enhancing of STAT3 and P-STAT3 protein expression in rats lung tissue.Conclusions：Lianggesan can prevent the abnormal expression of STAT3 and P-STAT3 in rats lung tissue during acute lung injury,and has a certain protective effect on ALI induced by lipopolysaccharide.