论文部分内容阅读
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 expression of α-actin in corpus cavernosum smooth muscle cells of diabetic erectile dysfunction rats. Methods Streptozotocin (STZ) was used to make models of diabetic and diabetic erectile dysfunction. Forty SPF SD male rats were randomly divided into two groups (20 rats in each group) The rats were divided into control group (5 rats without STZ injection) and diabetic model group with diabetic erectile dysfunction according to the factors of treatment, namely, STZ (60 mg / kg) given intraperitoneally to rats. Into the diabetic non-erectile dysfunction group, not a model group. The specimens of different treatment groups were studied for α-actin by immunohistochemical SP staining, and the myosin protein was detected by immunohistochemical SABC staining in different treated groups. The in situ hybridization was used to detect the difference Group osteopontin (OPN) mRNA content changes. Image Analysis Using a color image analysis system, a third person performed image analysis and data acquisition to measure the cumulative optical density (IOD) at each high magnification field of view. The IOD value was used to reflect the expression of the corresponding positive substance in the tissue sections. Results The IOD in diabetic erectile dysfunction group was lower than that in control group, non-erectile dysfunction group and non-diabetic model group (all P <0.05). The IOD in diabetic erectile dysfunction group was lower than that in control group and non-diabetic group (P <0.05) There was no significant difference in IOD between different time points (F = 3.801, P = 0.62). The interaction effect was not significant (F = 1.549, P = 0.225). There was no significant difference in IOD between different time points (F = 0.052, P = 0.821), IOD in each treatment group was not significantly different (F = 0.045, P = 0.987), but the interaction effect was not significant (F = 0.572, P = 0.639). There was no significant difference in IOD between OPN mRNA in situ hybridization staining at different time points (F = 1.288, P = 0.266), but the interaction effect was not significant (F = 1.819, P = 0.168) More than the other three groups (all P <0.001). IOD in diabetic non-erectile dysfunction group was higher than that in control group and non-model group (all P <0.001). There was no significant difference between control group and IOD group (P = 0.873). Conclusion Diabetes mellitus can cause the phenotypic transformation of the smooth muscle of the penis; cavernosal smooth muscle phenotype can lead to erectile dysfunction.