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作 者:孙小聪[1] 佟琳[1] 张媛莉[1] 陈韵名[1] 刘丽珍[1]
机构地区:[1]广东医学院附属医院重症医学科,广东湛江524000
出 处:《四川医学》2013年第6期740-742,共3页Sichuan Medical Journal
摘 要:目的研究脂多糖(lipopolysaccharide,LPS)诱导的急性肺损伤(Acute lung injury,ALI)大鼠肺组织中水通道蛋白(aquaporins,AQPs)AQP1、3表达的变化,探讨水通道蛋白1、3表达与急性肺损伤的关系。方法 40只SD大鼠随机分为LPS 2h组、LPS 6h组、LPS 12h组(LPS5mg/kg,用生理盐水稀释至2ml)和对照组(生理盐水2ml),每组10只(给药途径均通过鼠尾静脉)。分别在用药后2h、6h、12h用RT-PCR法检测肺组织AQPsmRNA表达。结果 LPS2h组AQP-1蛋白量表达开始下降,LPS6h组AQP-1蛋白量表达最低,LPS12h组接近正常水平。AQP-3的表达无明显变化。结论 AQP-1参与ALI液体的异常转运,可能与肺水肿的发病机制有关。AQP-3可能不参与ALI肺水肿的形成过程。Objective To study the expression of AQP-1 and AQP-3 in the pulmonary tissues of mice with acute lung injury induced by lipopolysaccharide and to clarify the relationship of ALI with the expression of AQP-1and AQP-3.Methods Forty healthy Sprague-Dawley mice were randomly divided into 4 groups:LPS 2h group,LPS 6h group,LPS 12h 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-1and AQP-3mRNA.Immunohistochemical method were used to determine the changes of AQP-1and AQP-3 protein in the pulmonary tissues of all the animals.Results Microscopic studies showed that there were not pathological changes in the lung tissue of rats in the control group.The most severest interstitial edema of lung and proliferation of epithelial cells were observed in the lung tissue of LPS6h group.The expression of AQP-1 mRNA were decreased in LPS2h group and significant reduction at LPS6h group(P0.05).The expression of AQP-3 mRNA had no obvious changes.Conclusion AQP-1 may play important roles in the abnormal ALI fluid transportation and might be assoiated with the development of pulmonary edema.AQP-3may not participate in the development of pulmonary edema during ALI.
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