Department of Urology, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Urology. 2013 May;81(5):1108.e7-14. doi: 10.1016/j.urology.2013.01.022. Epub 2013 Mar 22.
To prevent cavernous nerve injury and corpus cavernosum apoptosis-induced erectile dysfunction (ED) after prostatectomy surgery, we investigated whether oral administration of udenafil combination with covering adipose-derived stem cells (ADSCs) and brain-derived neurotrophic factor (BDNF) immobilized poly-lactic-co-glycolic (PLGA) membrane on the injured cavernous nerve could further improve erectile dysfunction.
Adult Sprague-Dawley rats were divided into 5 groups: normal group (sham-operated group), bilateral cavernous nerve injury (BCNI) group (BCNI group), udenafil group (oral administration of udenafil 20 mg/kg daily), AB group (BCNI group with ADSCs covered with BDNF membrane on cavernous nerve), AB/udenafil group (AB group with udenafil group). After 4 weeks, erectile function was examined before tissue harvest. Penile tissues were evaluated in terms of the expression of smooth muscle actin (SMA), neuronal nitric oxide synthase (nNOS), and vascular endothelial growth factor (VEGF). The cyclic guanosine monophosphate (cGMP) level of the corpus cavernosum was quantified by cGMP assay.
AB/udenafil treatment markedly improved erectile function and prevented the architecture damage of the corpus cavernosum, compared with other treated groups. Udenafil had no statistical significance on increasing nNOS expression, but enhanced VEGF expression. On the contrary, the AB group had no statistical significance on enhancing VEGF expression, but increased nNOS expression. AB/udenafil treatment significantly increased nNOS expression, VEGF expression, and elevated cGMP level, compared with the udenafil group and AB group.
The orally administered udenafil combination with ADSC/BDNF-membrane system protected cavernous nerve and improved angiogenesis in the corpus cavernosum, which further maintained erectile function in a rat model of postprostatectomy erectile dysfunction.
为了预防前列腺切除术后海绵体神经损伤和海绵体凋亡引起的勃起功能障碍（ED），我们研究了口服乌地那非联合覆盖脂肪源性干细胞（ADSCs）和脑源性神经营养因子（BDNF）固定在聚乳酸-共-羟基乙酸（PLGA）膜上对损伤的海绵体神经是否能进一步改善勃起功能障碍。
成年 Sprague-Dawley 大鼠分为 5 组：正常组（假手术组）、双侧海绵体神经损伤（BCNI）组（BCNI 组）、乌地那非组（口服乌地那非 20mg/kg 每日）、AB 组（BCNI 组用载有 BDNF 的 ADSCs 膜覆盖海绵体神经）、AB/乌地那非组（AB 组加用乌地那非）。4 周后，在组织采集前检查勃起功能。根据平滑肌肌动蛋白（SMA）、神经元型一氧化氮合酶（nNOS）和血管内皮生长因子（VEGF）的表达评估阴茎组织。通过 cGMP 测定定量测定海绵体的环鸟苷单磷酸（cGMP）水平。
AB/乌地那非治疗组与其他治疗组相比，显著改善了勃起功能，防止了海绵体的结构损伤。乌地那非对增加 nNOS 表达没有统计学意义，但增强了 VEGF 表达。相反，AB 组对增强 VEGF 表达没有统计学意义，但增加了 nNOS 表达。AB/乌地那非治疗组与乌地那非组和 AB 组相比，显著增加了 nNOS 表达、VEGF 表达和 cGMP 水平。
口服乌地那非联合 ADSC/BDNF 膜系统保护海绵体神经，改善海绵体血管生成，进一步维持前列腺切除术后勃起功能障碍大鼠模型的勃起功能。
