摘要
目的:了解降钙素基因相关肽(CGRP)对糖尿病性ED大鼠阴茎海绵体平滑肌细胞表型转化的影响。方法:利用链脲佐菌素建立糖尿病及糖尿病性ED大鼠模型。阴茎海绵体平滑肌细胞原代培养,并进行免疫细胞化学染色鉴定。实验分为2组:正常对照组和糖尿病性ED大鼠组。不同浓度(0、10,60,100 nmol/L)CGRP作用24h后,利用qRT-PCR检测各组细胞碱性调宁蛋白和骨桥蛋白mRNA的表达。结果:各组原代培养阴茎海绵体平滑肌细胞α-肌动蛋白阳性细胞率为(95.94±0.03)%。与正常对照组比较,糖尿病组ED大鼠阴茎海绵体平滑肌细胞碱性调宁蛋白mRNA表达显著减少(4.41±0.29 vs 10.35±0.62,P<0.01),而骨桥蛋白mRNA表达水平显著上调(5.28±0.32 vs 1.32±0.24,P<0.01)。当CGRP作用的终浓度为100 nmol/L时,糖尿病组大鼠阴茎海绵体平滑肌细胞经CGRP作用后,与未经其作用相比,碱性调宁蛋白mRNA表达显著上调(6.90±0.22 vs 4.41±0.29,P<0.01),而骨桥蛋白mRNA表达水平显著减少(3.26±0.31 vs 5.28±0.32,P<0.01)。结论:CGRP可使糖尿病性ED大鼠阴茎海绵体平滑肌细胞表型从合成型向收缩型转化。
Objective： To explore the effect of the calcitonin gene related peptide（CGRP） on the phenotypic transformation of corpus cavernosum smooth muscle cells（CCSM） in diabetic rats with erectile dysfunction（ED）.Methods： Models of diabetes and diabetic ED were established in male Sprague-Dawley rats by administration of streptozotocin,and CCSMs were primarily cultured and subjected to immunocytochemical assay.The cells were divided into a diabetic ED and a normal control group,and exposed to 0,10,60 and 100 nmol/L of CGRP for 24 hours.Then the relative expressions of calponin1（Cnn1） and osteopontin（OPN） mRNA were determined by real-time fluorescence quantitative RT-PCR（qRT-PCR）.Results： The rate of SMα-actin positive cells in the CCSMs was（95.94 ± 0.03） %.The expression of Cnnl mRNA was significantly lower while that of OPN mRNA remarkably higher in the diabetic ED rats（4.41 ± 0.29 and 5.28 ± 0.32） than in the normal controls（10.35 ± 0.62 and 1.32 ± 0.24）（P 0.01）.Exposure to 100 nmol/L of CGRP significantly upregulated the expression of Cnnl mRNA and downregulated that of OPN mRNA as compared with the unexposed rats（6.9 ± 0.22 vs 4.41 ± 0.29 and 3.26 ± 0.31 vs 5.28 ± 0.32,P 0.01）.Conclusion： CGRP can transform the phenotype of CCSMs in diabetic ED rats from contractile to synthetic type.
出处
《中华男科学杂志》
CAS
CSCD
北大核心
2011年第10期913-917,共5页
National Journal of Andrology
关键词
勃起功能障碍
表型转化
糖尿病
平滑肌细胞
erectile dysfunction
phenotype transformation
diabetes mellitus
smooth muscle cell
