Dai Yu-tian, Chen Yun, Yao Le-shen, Yang Rong, Sun Ze-yu, Wen Duan-gai
Department of Urology, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University School of Medicine, Nanjing, Jiangsu 210008, China.
Zhonghua Nan Ke Xue. 2005 Oct;11(10):748-51, 754.
To investigate the content of nerve growth factor (NGF) in penis of rats with diabetic erectile dysfunction (DED) and apply rhNGF to treat the DED rat model to study the pathogenesis mechanism of DED and treatment effects by NGF for DED rat model.
Fifty adult male SD rats were randomly selected to make up diabetic models. After 8 weeks, the mRNA and protein levels of NGF in rat penis were detected. Then the rest of rats were divided into 5 groups: normal control group, non-treated diabetes group, NGF treatment group, insulin treatment group, NGF plus insulin treatment group. After 8 weeks of treatment, intracavernous pressure (ICP) was measured. The content of neuronal nitric oxide synthase (nNOS) in the erectile tissue was also value- ated by immunohistochemistry staining.
Compared with those of normal control group, the mRNA content of NGF and protein in the penis of non-treated diabetic rats is increased significantly. Compared with non-treated diabetic group, ICP was much higher in the treated groups which received NGF or/and insulin therapy, and the changes in nNOS staining of those groups were the same.
The injury of pelvic splanchnic nerves in advanced stage of diabetes may lead to DED, which may be relevant to the abnormal of NGF level or the NGF receptors. The increased extent of NGF in penis of rat with DED suggests that erectile nerves be severely damaged by diabete and the increase of producing NGF couldn't compensate the needs for reproduction of the nerve fibers. The ability of combination of NGF with its receptor may also be damaged. It is helpful to use exogenous NGF to lessen the partly neuropathy and improve the erectile dysfunction of diabetic rats. The abnormal of NGF may play an important role in the pathogenesis of diabetic ED and its treatment.
探讨糖尿病性勃起功能障碍(DED)大鼠阴茎中神经生长因子(NGF)的含量,并应用重组人神经生长因子(rhNGF)治疗DED大鼠模型,以研究DED的发病机制及NGF对DED大鼠模型的治疗作用。
随机选取50只成年雄性SD大鼠制备糖尿病模型。8周后,检测大鼠阴茎中NGF的mRNA和蛋白水平。然后将其余大鼠分为5组:正常对照组、糖尿病未治疗组、NGF治疗组、胰岛素治疗组、NGF加胰岛素治疗组。治疗8周后,测量海绵体内压(ICP)。同时采用免疫组织化学染色法评估勃起组织中神经元型一氧化氮合酶(nNOS)的含量。
与正常对照组相比,糖尿病未治疗组大鼠阴茎中NGF的mRNA含量和蛋白水平显著升高。与糖尿病未治疗组相比,接受NGF或/和胰岛素治疗的组ICP明显升高,且这些组nNOS染色的变化相同。
糖尿病晚期盆腔内脏神经损伤可能导致DED,这可能与NGF水平或NGF受体异常有关。DED大鼠阴茎中NGF升高表明糖尿病严重损害了勃起神经,NGF生成增加无法满足神经纤维再生的需求。NGF与其受体结合的能力也可能受损。外源性NGF有助于减轻部分神经病变,改善糖尿病大鼠的勃起功能障碍。NGF异常可能在糖尿病性勃起功能障碍的发病机制及其治疗中起重要作用。