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水通道蛋白1、3、4、5在内毒素性急性肺损伤小鼠肺组织中的表达
李波1,2,陈东2,王桂芳1,董春玲1,王向东1*,,白春学1*
0
(1.复旦大学附属中山医院呼吸内科,上海 200032; 2.吉林大学基础医学院组织学与胚胎学教研室,长春 130021)
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: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 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8 h 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。
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).
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 AQP1,AQP3,AQP4 and AQP5 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 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. ALI 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 mRNA. Immunohistochemical 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 ALI 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.
Key words:  acute lung injury  pulmonary edema  aquaporins  lipopolysaccharide