海绵体神经损伤后阴茎组织氧化应激的变化

Changes in oxidative stress in rat penis after bilateral cavernous nerve crashed injury

目的探讨大鼠双侧海绵体神经(CN)钳夹损伤后阴茎组织氧化应激的变化规律。方法 56只SD雄性大鼠随机均分成假手术组、双侧CN钳夹损伤组。分别于术后第1、2、4、12周每组7只大鼠分别取阴茎组织采用蛋白印迹法来检测谷胱甘肽过氧化物酶(GPX)及3-硝基酪氨酸(NT-3)的蛋白表达水平。术后12周进行电刺激CN来观察海绵体内压的变化以反映其勃起功能,随后取CN干进行甲苯胺蓝染色观察有髓鞘轴突的数目变化以了解神经再生情况。结果与假手术组相比,钳夹损伤组GPX表达在术后第1周和2周明显增加(P<0.05),在术后第4及12周基本下降至正常水平;NT-3表达在术后第1、2、4周明显增加(P<0.05),在术后第12周基本下降至正常水平。术后3个月,钳夹损伤组最大海绵体内压为(52.4±11.2)cmH2O,明显低于假手术组(102.5±9.0)cmH_2O(P<0.05)。甲苯胺蓝染色显示损伤组的有髓鞘轴突为(59.9±15.9)个,明显低于假手术组(180.6±27.7,P<0.05)。结论海绵体神经钳夹损伤后早期阴茎组织氧化应激反应明显,提示在海绵体神经损伤后勃起功能障碍的发病过程中,氧化应激起重要作用。

Objective To investigate the changes in oxidative stress in rat penis after bilateral cavernous nerre（CN） crashed injury. Methods A total of 56 Sprague-Dawley male adult rats were randomly divided into 2 groups：sham operation group （n = 28, sham group） and bilateral cavernous nerve crashed injury group （n = 28, CN-crushed group）. Glutathione peroxidase （GPX） protein expression and nitrotyrosine-3 （NT-3） levels in penile tissues were measured in week 1, 2, 4, and 12 after operation. Erectile function was assessed by cavernous nerve electrostimulation, and nerve regeneration was assessed by toluidine blue staining of CN in week 12. Results In week 1 and 2 after operation, GPX protein expression was significantly increased in CN-crushed group （P〈0.05） compared with the sham group. However, it decreased to normal level in both groups in week 4 and 12. In week 1, 2, and 4, the NT-3 level was significantly increased in CN-crushed group （P〈0.05） compared with the sham group. However, it decreased to normal level in both groups in week 12. The mean maximal intracavernous pressure （ICP） in CN-crushed group （52.4±11.2） cmH20 was significantly lower than in the sham group （102.5 ± 9.0, P 〈 0.05） in week 12 after operation. Meanwhile, the CN-crushed group had fewer myelinated axons of CNs （59.9 ±15.9） than the sham group （180.6±27.7,P〈0.05）. Conclusion The level of oxidative stress in penis increases obviously in the early stage after bilateral cavernous nerve crushed injury, indicating that oxidative stress plays an important role in injured CNs.