【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。更多还原

【Abstract】 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 tmmunohistoehemistry and color image analysis were used to observe the expression of oL-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 eavernosum 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 can be caused by phenotype modulation of smooth muscle in corpus cavernosum.更多还原