Wei An-Yang, Cheng Yi, Li Yu-Gang
Department of Urological Surgery; Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zhonghua Yi Xue Za Zhi. 2007 Nov 13;87(42):3006-11.
To investigate the phenotype modulation of smooth muscle of corpus cavernosum in diabetes mellitus with erectile dysfunction.
Thirty SD rats were randomly divided into 2 equal groups: 4-week group and 7-week group, injected with streptozocin to cause diabetes mellitus (DM), and then subdivided into DM group [with DM and without erectile dysfunction. (ED)], DM + ED group (with DM and ED), and group of failure to cause DM (Group None) according whether DM was induced. Another 10 rats without STZ injection were divided into 4-week and 7-week control groups. The penis was resected and immunohistochemistry and color image analysis were used to observe the expression of alpha-actin and desmin in the corpus cavernosum. In situ hybridization was used to detect the mRNA expression of osteopontin (OPN), characteristic of noncontractil phenotype.
The alpha-actin expression of smooth muscle in corpus cavernosum in the DM + ED group was significantly lower than those of the other groups (all P < 0.05). No significant difference existed between the 7 week group and 4 week group (F = 3.801, P = 0.62), and there was significant interaction (F = 1.549, P = 0.225). There was no significant difference in the desmin expression of smooth muscle in corpus cavernosum among different groups (F = 0.045, P = 0.987) and there was not significant interaction (F = 0.572, P = 0.639). The OPN mRNA expression of smooth muscle in corpus cavernosum of the DM + ED group was significantly higher than those of the other subgroups (F = 156.439, P = 0.000). No significant difference existed between the 7 week group and 4 week group (F = 1.288, P = 0.266), and there was no significant interaction (F = 1.819, P = 0.168).
Phenotype modulation of smooth muscle in corpus cavernosum can be caused by DM. ED can be caused by phenotype modulation of smooth muscle in corpus cavernosum.
研究糖尿病伴勃起功能障碍患者阴茎海绵体平滑肌的表型调节。
将30只SD大鼠随机分为两组,每组15只:4周组和7周组,注射链脲佐菌素诱导糖尿病(DM),然后根据是否诱导出DM再细分为DM组[患有DM但无勃起功能障碍(ED)]、DM + ED组(患有DM和ED)和未诱导出DM组(无DM组)。另外10只未注射链脲佐菌素的大鼠分为4周和7周对照组。切除阴茎,采用免疫组织化学和彩色图像分析观察阴茎海绵体中α-肌动蛋白和结蛋白的表达。采用原位杂交检测骨桥蛋白(OPN)的mRNA表达,OPN是非收缩表型的特征。
DM + ED组阴茎海绵体平滑肌α-肌动蛋白表达明显低于其他组(均P < 0.05)。7周组和4周组之间无显著差异(F = 3.801,P = 0.62),且存在显著交互作用(F = 1.549,P = 0.225)。不同组阴茎海绵体平滑肌结蛋白表达无显著差异(F = 0.045,P = 0.987),且无显著交互作用(F = 0.572,P = 0.639)。DM + ED组阴茎海绵体平滑肌OPN mRNA表达明显高于其他亚组(F = 156.439,P = 0.000)。7周组和4周组之间无显著差异(F = 1.288,P = 0.266),且无显著交互作用(F = 1.819,P = 0.168)。
DM可导致阴茎海绵体平滑肌表型调节。阴茎海绵体平滑肌表型调节可导致ED。