中文摘要：

目的：研究脂多糖（lipopolysaccharide,LPS）诱导的急性肺损伤（ALI）小鼠肺组织中水通道蛋白（AQP）1、3、4、5的表达变化,探讨水通道蛋白1、3、4、5表达与急性肺损伤的关系。方法：40只健康雄性的C57BL/6小鼠随机分为LPS4h组、LPS6h组、LPS8h组、LPS10h组（以LPS诱导ALI模型）和对照组,每组8只。采用实时定量PCR测定小鼠AQP-1、AQP-3、AQP-4和AQP-5 mRNA表达,免疫组化和Western印迹法观察AQP-1、AQP-3、AQP-4和AQP-5蛋白表达,同时进行肺湿/干重比值测定以及肺组织病理染色。结果：LPS4h、6h、8h、10h组肺湿/干重比值（4.39±0.19、4.58±0.17、4.87±0.21、5.28±0.16）明显高于对照组（3.99±0.25,P〈0.05）。LPS灌注后4h AQP-1蛋白量减少至对照组的（74.1±5.2）%,AQP-5降至对照组的（70.3±7.1）%;LPS灌注后8h AQP-1蛋白量减少至对照组的（45.2±4.4）%,AQP-5降至对照组的（38.6±8.9）%。AQP-3和AQP-4的表达没有明显变化。结论：AQP-1和AQP-5可能参与ALI液体的异常转运,可能与肺水肿的发病机制有关。AQP-3和AQP-4可能不参与ALI肺水肿的形成过程。

英文摘要：

Obieetive：To study the expression of AQP-1 ,AQP-3,AQP-4 and AQP-5 in the pulmonary tissues of mice with acute lung injury （ALl） induced by lipopolysaccharide （LPS） and to clarify the relationship of ALl with the expression of AQP-1,AQP-3,AQP-4 and AQP-5. Methods.. Forty healthy male C57BL/6 mice were evenly randomized into 5 groups： LPS 4 h group,LPS 6 h group,LPS 8 h group,LPS 10 h group and control group. ALl model was induced with LPS in all the LPS groups. Real-time PCR was used to observe the expression changes of AQP-1,AQP-3,AQP-4 and AQP-5 rnRNA. Irnmunohistochemical method and Western blotting assay were used to determine the changes of AQP-1 ,AQP-3, AQP-4 and AQP-5 protein in the pulmonary tissues of all the animals. Meanwhile,measurement of lung wet/dry （W/D） weight ratio and pathological staining were performed in each group. Results： The W/D values of the LPS 4 h,6 h,8 h and 10 h groups （4.39±0. 19,4.58± 0.17,4. 87±0. 21 and 5. 28 ± 0. 16, respectively） were significantly higher than that of the control group （3. 99 ± 0. 25, all P〈0.05）. The expression of AQP-1 and AQP-5 protein in the lung of the LPS 4 h group decreased to （74. 1 ±5.2）% and （70.3±7.1）% that of the control group; the expression of AQP-1 and AQP-5 protein in the lung of the LPS 8 h group decreased to （45.2±4.4）% and （38. 6 ±8. 9）% that of the control group, and the expression of AQP-3 and AQP-4 had no obvious changes. Conclusion： AQP-1 and AQP-5 may play important roles in the abnormal ALl fluid transportation and might be associated with the development of pulmonary edema. AQP-3 and AQP-4 may not participate in the development of pulmonary edema during ALI.