| 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LPS 4 h组、LPS 6 h组、LPS 8 h组、LPS 10 h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AQP1、AQP3、AQP4和AQP5 mRNA表达，免疫组化和Western印迹法观察AQP1、AQP3、AQP4和AQP5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：LPS 4 h、6 h、8 h、10 h 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4 h AQP1蛋白量减少至对照组的（74.1±5.2）%，AQP5降至对照组的（70.3±7.1）%；LPS 灌注后8 h AQP1 蛋白量减少至对照组的（45.2±4.4）%，AQP5降至对照组的（38.6±8.9）%。AQP3和AQP4的表达没有明显变化。结论：AQP1和AQP5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。AQP3和AQP4可能不参与ALI肺水肿的形成过程。 |
| 关键词: 急性肺损伤 肺水肿 水通道蛋白 脂多糖 |
| DOI：10.3724/SP.J.1008.2008.00131 |
| 投稿时间：2007-10-19修订日期：2007-12-07 |
| 基金项目:国家自然科学基金(30370611) ；上海市科学技术委员会资助项目（LJ06022）; 上海市重点学科建设项目（B115）. |
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| Expression of AQP 1, AQP 3, AQP 4 and AQP 5 in pulmonary tissues of mice with endotoxin induced acute lung injury |
| LI Bo1,2,CHEN Dong2,WANG Gui-fang1,DONG Chun-ling1,WANG Xiang-dong1*,BAI Chun-xue1* |
| (1.Department of Respiratory Medicine,Zhongshan Hospital,Fudan University,Shanghai 200032,China; 2.Department of Histology and Embryology,College of Basic Medical Sciences,Jilin University,Changchun 130021) |
| Abstract: |
| Objective：To study the expression of AQP1,AQP3,AQP4 and AQP5 in the pulmonary tissues of mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS) and to clarify the relationship of ALI with the expression of AQP1,AQP3,AQP4 and AQP5. 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. ALI model was induced with LPS in all the LPS groups. Realtime PCR was used to observe the expression changes of AQP1,AQP3,AQP4 and AQP5 mRNA. Immunohistochemical method and Western blotting assay were used to determine the changes of AQP1,AQP3,AQP4 and AQP5 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 AQP1 and AQP5 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 AQP1 and AQP5 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 AQP3 and AQP4 had no obvious changes. Conclusion: AQP1 and AQP5 may play important roles in the abnormal ALI fluid transportation and might be associated with the development of pulmonary edema. AQP3 and AQP4 may not participate in the development of pulmonary edema during ALI. |
| Key words: acute lung injury pulmonary edema aquaporins lipopolysaccharide |
