中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2010年
10期
1332-1336
,共5页
李又空%张先觉%杨光华%周家杰%丁坤%王建国%朱敏%陈忠军%曾金敏%廖义翔
李又空%張先覺%楊光華%週傢傑%丁坤%王建國%硃敏%陳忠軍%曾金敏%廖義翔
리우공%장선각%양광화%주가걸%정곤%왕건국%주민%진충군%증금민%료의상
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
輸尿管梗阻/代謝%腎/代謝%水通道蛋白質1/代謝%水通道蛋白質2/代謝%尿△/生理學
수뇨관경조/대사%신/대사%수통도단백질1/대사%수통도단백질2/대사%뇨△/생이학
Ureteral obstruction/ME%Kidney/ME%Aquaporin 1/ME%Aquaporin 2/ME%URINE △/PH
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.
目的 探討單側輸尿管梗阻解除前後腎髒水通道蛋白(AQP)變化與尿液濃縮功能障礙之間的聯繫.方法 56隻體重180～200 g成年雄性SD大鼠隨機分為實驗組(n=48隻)和對照組(n=8隻).實驗組大鼠通過手術建立單側輸尿管梗阻模型併于相應時間點解除梗阻,對照組接受假手術.于相應時間點檢測尿液滲透壓改變,處死動物取齣腎髒後通過Western blot檢測梗阻前後AQP1、AQP2蛋白錶達的變化,免疫組化觀察蛋白錶達部位.結果 梗阻後1、2 d及解除梗阻後1d,患側AQP1、AQP2的錶達隨時間延長進行性下降,解除梗阻後7d其錶達有所迴升,AQP2于梗阻解除後14 d內恢複正常水平,而AQP1則在梗阻解除後21 d內達到正常水平.同時AQPs的變化趨勢與患側尿液滲透壓改變趨勢相同.梗阻解除前AQP2分佈于集閤管主細胞的胞漿及管週膜,解除梗阻後其錶達更多的集中于管週膜.結論 AQP錶達下降是造成梗阻性腎積水中尿液濃縮功能障礙的重要原因,同時梗阻解除後AQP2接受ADH的調節.
목적 탐토단측수뇨관경조해제전후신장수통도단백(AQP)변화여뇨액농축공능장애지간적련계.방법 56지체중180～200 g성년웅성SD대서수궤분위실험조(n=48지)화대조조(n=8지).실험조대서통과수술건립단측수뇨관경조모형병우상응시간점해제경조,대조조접수가수술.우상응시간점검측뇨액삼투압개변,처사동물취출신장후통과Western blot검측경조전후AQP1、AQP2단백표체적변화,면역조화관찰단백표체부위.결과 경조후1、2 d급해제경조후1d,환측AQP1、AQP2적표체수시간연장진행성하강,해제경조후7d기표체유소회승,AQP2우경조해제후14 d내회복정상수평,이AQP1칙재경조해제후21 d내체도정상수평.동시AQPs적변화추세여환측뇨액삼투압개변추세상동.경조해제전AQP2분포우집합관주세포적포장급관주막,해제경조후기표체경다적집중우관주막.결론 AQP표체하강시조성경조성신적수중뇨액농축공능장애적중요원인,동시경조해제후AQP2접수ADH적조절.
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.
