糖尿病性勃起功能障碍大鼠阴茎海绵体平滑肌细胞α-肌动蛋白的表达及意义  

Phenotype modulation of smooth muscle in corpus cavernosum in penis tunica albuginea in diabetes mellitus with erectile dysfunction:experiment with rats

作　　者：韦安阳[1] 程祎[1] 李煜罡[1] 

机构地区：[1]南方医科大学附属南方医院惠侨楼泌尿外科,广州510515

出　　处：《中华医学杂志》2007年第42期3006-3011,共6页National Medical Journal of China

摘　　要：目的了解糖尿病性勃起功能障碍大鼠阴茎海绵体平滑肌细胞α-肌动蛋白(actin)的表达及意义。方法利用链脲佐菌素(STZ)制作糖尿病及糖尿病性勃起功能障碍模型,40只 SPF 级SD 雄性大鼠,先按时间随机分为两组(每组20只),分别是注射 STZ 后7周组和4周组,再按处理因素即给予大鼠腹腔注射 STZ(60 mg/kg)是否成模,分为对照组(未注射 STZ,5只)、成糖尿病性勃起功能障碍模型组、成糖尿病性非勃起功能障碍组、未成模组。利用免疫组化 SP 染色法对不同处理组的标本进行α-肌动蛋白的研究,利用免疫组化 SABC 染色法对不同处理组的标本进行肌间线蛋白的研究,利用原位杂交技术检测不同组别骨桥蛋白(OPN)mRNA 含量的改变。图像分析利用彩色图文分析系统,第三人进行图像分析及数据采集,测量随机每高倍镜视野下累积光密度(IOD),以 IOD 的值反映组织切片中相应阳性物质的表达程度。结果糖尿病性勃起功能障碍组 IOD 均小于对照组、糖尿病非勃起功能障碍组及未成模组(均 P<0.05),糖尿病非勃起功能障碍组的 IOD 小于对照组和未成模组(P<0.05),不同时间点间的 IOD 不存在显著性差异(F=3.801,P=0.62),交互效应不显著(F=1.549,P=0.225)。免疫组化染色不同时间点间的 IOD 不存在显著性差异(F=0.052,P=0.821),各处理组间的 IOD 不存在显著性差异(F=0.045,P=0.987),交互效应不显著(F=0.572,P=0.639)。OPN mRNA 原位杂交染色不同时间点间的 IOD 不存在显著性差异(F=1.288,P=0.266),交互效应不显著(F=1.819,P=0.168),糖尿病性勃起功能障碍组的 IOD 均大于其余三组(P 均<0.001)。糖尿病非勃起功能障碍组的 IOD 大于对照组和未成模组(P 均<0.001)。对照组的 IOD 与未成模组未见显著差异(P=0.873)。结论糖尿病可以引起阴茎海绵体平滑肌的表型转化;阴茎海绵体平滑肌表型转化可以导致勃起功能障碍。Objective To investigate the phenotype modulation of smooth muscle of corpus cavernosum in diabetes mellitus with erectile dysfunction. Methods 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 tmmunohistochemistry and color image analysis were used to observe the expression of α-actin and desmin in the corpus cavernosum. In situ hybridization was used to detect the mRNA expression of osteopontin （ OPN ）, characteristic of noncontractil phenotype. Results The α-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 ）. Conclusion Phenotype modulation of smooth muscle in corpus cavernosum can be caused by DM ED carl be caused by phenotype modulation of smooth muscle in corpus cavernosum.

关 键 词：糖尿病 勃起功能障碍 阴茎海绵体平滑肌细胞 Α-肌动蛋白 表达 意义 表型转化 

分 类 号：R698[医药卫生—泌尿科学]