摘要
目的探讨糖尿病性勃起功能障碍(DED)大鼠阴茎海绵体组织形态学及平滑肌Q-SMA表达量的变化。方法建立DED大鼠模型,取阴茎海绵体组织,应用Masson三色法检测平滑肌/胶原纤维相对含量;用免疫荧光染色法检测Q平滑肌肌动蛋白(α-SMA)的表达情况。结果DED组大鼠平滑肌/胶原纤维比值(0.15±0.05)明显低于和对照组大鼠(0.21±0.06,P〈0.05)。DED组Q.SMA蛋白平均光密度值为0.24±0.20,明显低于对照组0.52±0.33,差异具统计学意义(P〈0.05)。结论DED大鼠阴茎海绵体平滑肌细胞数量减少、胶原纤维密度增加、海绵体平滑肌细胞由收缩型向合成型转化,可能是DED的发病机制之一。
Objective To investigate histology morphology and a -SMA expression in smooth muscle in corpus cavernosum of rats with diabetic erectile dysfunction(DED). Methods SD rat models with DED were established by intraperitoneal injection of streptozotocin (STZ). The density of collage fibrin in corpus cavernosum was measured by Masson staining, and the expression of α -SMA was measured by fluorescence immunohistochemistry. Results Compared with that of the controls, the ratio of smooth muscle cell (SMC) and collagen significantly decreased in the DED group (0.21±0.06 vs 0.15±0.05, P〈0.05),and the expression of a -SMA in the penile smooth muscle cells also decreased obviously in the DED group (0.52±0.33 vs 0.24±0.20, P〈0.05). Conclusion Decrease in the amount of SMCs and increase in the density of collagen fibrin faciliating the SMCs from contraction phenotype into synthetic phenotype, which might be one of the pathogenesis of DED.
出处
《中国男科学杂志》
CAS
CSCD
北大核心
2013年第2期17-20,共4页
Chinese Journal of Andrology
基金
基金项目资助:国家自然科学基金资助项目(81070487)
教育部博士点新教师基金(20090171120078)
广东省自然科学基金资助项目(S2012010009140)
广东省科技计划项目基金(20108031600038)
广东省医学科研基金资助项目(A2009190)
高校基本科研业务费中山大学青年教师培育项目(09ykpy14):AsiaPacificSocietyforSexualMedicineResearchGrant(2008-2)
PfizerAsiaUrologyResearchGrant(WS570255)