膀胱出口梗阻后逼尿肌过度活动对大鼠膀胱水通道蛋白和一氧化氮合酶表达的影响。
Effect of detrusor overactivity on the expression of aquaporins and nitric oxide synthase in rat urinary bladder following bladder outlet obstruction.
作者信息
Kim Sun-Ouck, Choi Dongjune, Song Seung Hee, Ahn Kyu Youn, Kwon Dongdeuk, Park Kwangsung, Ryu Soo Bang
机构信息
Department of Urology, Chonnam National University Medical School, Gwangju, Korea;
出版信息
Can Urol Assoc J. 2013 May-Jun;7(5-6):E268-74. doi: 10.5489/cuaj.993.
BACKGROUND
Aquaporins (AQPs) have recently been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play a role in the bladder overactivity related to bladder outlet obstruction (BOO). The purpose of this study is to investigate the effect of BOO on the expression of AQP2-3 and nitric oxide synthase (NOS) isoforms in rat urothelium.
METHODS
Female Sprague-Dawley rats (230-240 g, n = 60) were divided into 2 groups. The control group (n = 30) and the partial bladder outlet obstruction (BOO) group (n = 30). After 4 weeks, we performed a urodynamic study to measure the contraction interval and contraction pressure. The expression and cellular localization of AQP2-3, endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) were determined by Western blot and immunohistochemistry.
RESULTS
On the cystometrogram, the estimated contraction interval time (minutes, mean ± SE) was significantly lower in the BOO group (3.0 ± 0.9) than in the control group (6.3 ± 0.4; p < 0.05). AQP2 was localized in the cytoplasm of the epithelium, whereas AQP3 was found only in the cell membrane of the epithelium. The protein expression of AQP2-3, eNOS and nNOS was significantly increased in the BOO group.
CONCLUSION
Detrusor overactivity induced by BOO causes a significant increase in the expression of AQP2-3, eNOS, and nNOS in rat urinary bladder. This may imply that the AQPs and NOS isoforms have a functional role in the bladder dysfunction that occurs in association with BOO.
背景
水通道蛋白（AQPs）最近被报道在大鼠和人类尿路上皮中表达。一氧化氮（NO）被认为在与膀胱出口梗阻（BOO）相关的膀胱过度活动中起作用。本研究的目的是探讨BOO对大鼠尿路上皮中AQP2 - 3和一氧化氮合酶（NOS）亚型表达的影响。
方法
将雌性Sprague - Dawley大鼠（230 - 240 g，n = 60）分为2组。对照组（n = 30）和部分膀胱出口梗阻（BOO）组（n = 30）。4周后，我们进行了尿动力学研究以测量收缩间隔和收缩压力。通过蛋白质印迹法和免疫组织化学法测定AQP2 - 3、内皮型一氧化氮合酶（eNOS）和神经元型一氧化氮合酶（nNOS）的表达及细胞定位。
结果
在膀胱压力容积图上，BOO组的估计收缩间隔时间（分钟，平均值±标准误）显著低于对照组（3.0±0.9），对照组为（6.3±0.4；p < 0.05）。AQP2定位于上皮细胞的细胞质中，而AQP3仅在上皮细胞膜中发现。BOO组中AQP2 - 3、eNOS和nNOS的蛋白质表达显著增加。
结论
BOO诱导的逼尿肌过度活动导致大鼠膀胱中AQP2 - 3、eNOS和nNOS的表达显著增加。这可能意味着AQPs和NOS亚型在与BOO相关的膀胱功能障碍中具有功能性作用。
Zotero 插件