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作 者:李又空[1] 张先觉[1] 杨光华[1] 周家杰[1] 丁坤[1] 王建国[1] 朱敏[1] 陈忠军[1] 曾金敏[1] 廖义翔[1]
机构地区:[1]华中科技大学同济医学院附属荆州市中心医院泌尿外科,湖北省荆州434020
出 处:《中国医师杂志》2010年第10期1332-1336,共5页Journal of Chinese Physician
摘 要:目的 探讨单侧输尿管梗阻解除前后肾脏水通道蛋白(AQP)变化与尿液浓缩功能障碍之间的联系.方法 56只体重180~200 g成年雄性SD大鼠随机分为实验组(n=48只)和对照组(n=8只).实验组大鼠通过手术建立单侧输尿管梗阻模型并于相应时间点解除梗阻,对照组接受假手术.于相应时间点检测尿液渗透压改变,处死动物取出肾脏后通过Western blot检测梗阻前后AQP1、AQP2蛋白表达的变化,免疫组化观察蛋白表达部位.结果 梗阻后1、2 d及解除梗阻后1d,患侧AQP1、AQP2的表达随时间延长进行性下降,解除梗阻后7d其表达有所回升,AQP2于梗阻解除后14 d内恢复正常水平,而AQP1则在梗阻解除后21 d内达到正常水平.同时AQPs的变化趋势与患侧尿液渗透压改变趋势相同.梗阻解除前AQP2分布于集合管主细胞的胞浆及管周膜,解除梗阻后其表达更多的集中于管周膜.结论 AQP表达下降是造成梗阻性肾积水中尿液浓缩功能障碍的重要原因,同时梗阻解除后AQP2接受ADH的调节.Objective To investigate the change of AQP1 and AQP2 before and after the release of obstruction and explore the relationship between reabsorption dysfunction of renal tubule and the change of AQPs. Methods The model of unilateral ureter obstruction (UUO) was established by surgery. Western blot and immunohistochemistry were used to study the expression of AQPs before and after obstruction. Results In UUO model, both AQPs began to down-regulate one day after obstruction, the expression of both AQPs became lower one day after the release of obstruction. And they started to up-regulate 7 day after the release of obstruction. AQP2 became normal since 14 days after the release of obstruction, and AQP1 became normal since 21 days after the release of obstruction. Conclusion The expression of AQP1 and AQP2 were descended in hydronephrosis. The dysfunction of renal tubule and the osmotic-dependent polyuria after the release of obstruction in UUO were caused by the down - regulation of AQPs.
关 键 词:输尿管梗阻/代谢 肾/代谢 水通道蛋白质1/代谢 水通道蛋白质2/代谢 尿△/生理学
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