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首页> 外文期刊>The journal of sexual medicine >A mouse model of cavernous nerve injury-induced erectile dysfunction: functional and morphological characterization of the corpus cavernosum.
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A mouse model of cavernous nerve injury-induced erectile dysfunction: functional and morphological characterization of the corpus cavernosum.

机译：海绵体神经损伤引起的勃起功能障碍的小鼠模型：海绵体的功能和形态特征。

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INTRODUCTION: With the advent of genetically engineered mice, it seems important to develop a mouse model of cavernous nerve injury (CNI). AIM: To establish a mouse model of CNI induced either by nerve crushing or by neurectomy and to evaluate time-dependent derangements in penile hemodynamics in vivo and subsequent histologic alterations in the cavernous tissue. METHODS: Twelve-week-old C57BL/6J mice were divided into 4 groups (N=36 per group): control, sham operation, bilateral cavernous nerve crush, and bilateral cavernous neurectomy group. MAIN OUTCOME MEASURES: Three days and 1, 2, 4, 8, and 12 weeks after CNI, erectile function was measured by electrical stimulation of the cavernous nerve. The penis was then harvested and TUNEL was performed. Immunohistochemical analysis was performed assaying for caspase-3, transforming growth factor-beta1 (TGF-beta1), phospho-Smad2, PECAM-1, factor VIII, and smooth muscle alpha-actin. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in endothelial cells or smooth muscle cells were counted. RESULTS: Erectile function was significantly less in the cavernous nerve crushing and neurectomy groups than in the control or sham group. This difference was observed at the earliest time point assayed (day 3) and persisted up to 4 weeks after nerve crushing and to 12 weeks after neurectomy. The apoptotic index peaked at 1 or 2 weeks after CNI and decreased thereafter. Cavernous TGF-beta1 and phospho-Smad expression was also increased after CNI. The numbers of apoptotic cells and phospho-Smad2-immunopositive cells in cavernous endothelial cells and smooth muscle cells were significantly greater in the cavernous nerve crush and cavernous neurectomy groups than in the control or sham group. Conclusion. The mouse is a useful model for studying pathophysiologic mechanisms involved in erectile dysfunction after CNI. Early intervention to prevent apoptosis in smooth muscle cells and endothelial cells or to inhibit cavernous tissue fibrosis is required to restore erectile function.
机译：简介：随着基因工程小鼠的出现，建立海绵状神经损伤（CNI）的小鼠模型似乎很重要。目的：建立通过神经压迫或神经切除术诱导的CNI小鼠模型，并评估体内阴茎血流动力学的时间依赖性紊乱以及随后海绵组织的组织学改变。方法：将12周龄的C57BL / 6J小鼠分为4组（每组N = 36）：对照组，假手术，双侧海绵体神经压迫和双侧海绵体神经切除术组。主要观察指标：CNI后三天，1、2、4、8和12周，通过电刺激海绵状神经测量勃起功能。然后收获阴茎并进行TUNEL。进行了免疫组织化学分析，分析了caspase-3，转化生长因子-beta1（TGF-beta1），磷酸-Smad2，PECAM-1，因子VIII和平滑肌α-肌动蛋白。计数内皮细胞或平滑肌细胞中的凋亡细胞和磷酸化Smad2-免疫阳性细胞的数目。结果：海绵体神经压迫和神经切除术组的勃起功能明显低于对照组或假手术组。这种差异在最早检测到的时间点（第3天）观察到，并持续持续到神经压迫后4周和神经切除术后12周。凋亡指数在CNI后1或2周达到峰值，此后下降。 CNI后，海绵状TGF-beta1和磷酸Smad表达也增加。海绵状神经挤压和海绵状神经切除术组中，海绵状内皮细胞和平滑肌细胞中凋亡细胞和磷酸化Smad2免疫阳性细胞的数量明显多于对照组或假手术组。结论。小鼠是研究CNI后勃起功能障碍的病理生理机制的有用模型。需要早期干预以防止平滑肌细胞和内皮细胞凋亡或抑制海绵状组织纤维化，以恢复勃起功能。

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