中文摘要：

目的：探讨凉膈散对脂多糖诱导大鼠急性肺损伤肺水肿及肺水通道蛋白（aquaporin，AQP）1、5表达的影响。方法：大鼠随机分成LPS组、LPS＋三个不同剂量凉膈散组、LPS＋地塞米松组、对照组，LPS造模动物，又分为注射IJPS后1、2、4、8、16h不同时相处死组。各组大鼠在相应时间点处死后取肺组织测定大鼠肺水含量、肺系数以及观察肺组织形态学的改变，采用蛋白免疫印迹分析（Westernblot）法和免疫组化法（SP）检测大鼠肺组织中AQP-l、AQP-5蛋白表达和分布情况。结果：与对照组相比，LPs组大鼠致损伤后2h，肺水含量、肺系数持续增高，肺组织内AQP-1、AQP-5表达开始下降，损伤4h后，AQP-l表达略有回升，而AQP-5表达随着损伤时间的延长持续降低；病理形态学显示肺泡隔增厚、肺间质及肺泡水肿，并有大量炎性细胞的浸润。与LPS组比较，凉膈散各剂量及地塞米松干预组大鼠病理损伤明显减轻，肺水含量、肺系数值显著降低（P〈0．05，P〈0．01），肺组织内AQP-1、AQP-5表达显著增加（P〈0．05，P〈0．01）。结论：凉膈散对内毒素诱导的大鼠急性肺损伤肺水肿有保护作用，其机制可能与上调急性肺损伤时肺组织内AQP-1、AQP-5蛋白的表达有关。

英文摘要：

To investigate the effects of Lianggesan on the acute pulmonary edema on rats induced by the lipopolysaccharide and impact of it on the expression of acauprin 1 and 5. Methods ： The rats were randomly assigned into three groups ： LPS group, LPS combined plus Li- anggesan of various dosage, LPS plus dexamethasone group, and control group. Rat with LPS induced acute pulmonary edema were further di- vided into five groups according to the＇time interval between the injection of LPS and sacrifice（ 1,2,4, 8,16 h）. Lung tissues were taken form the rats being executed at various time intervals, which was then used for measurement of contents of water, lung index, and observation of morphological change;Western blot and immunohistochemistry were run for detecting the distribution and expression of AQP-1 and AQP-5. Results ： When compared to the control group,the pulmonary water content and lung index rose continuously, the expression of AQP-1 and AQP-5 declined ;4 hours after the induced injury, the expression of AQP-I was slightly increased, while the expression of APQ-5 continued to decline. Compared to LPS group, group of various lianggesan doses and dexamethasone-treated group exhibited obviously abated tissue dam- age, with pulmonary water content and lung index significantly reduced （ P 〈 0.05, P 〈 0.01 ）, and expression of AQP-I and AQP-5 increasing significantly（ P 〈 0.05 ,P 〈 0.01 ）. Conclusion： Lianggesan can relieve for endotoxin-induced pulmonary damage in rats, the mechanism of which possibly resides oll promotion of the expression of proteins AQP-1 and AQP-5.