摘要
目的:研究大鼠糖尿病时睾丸的主要病理变化及对间质细胞(Leydig细胞)睾酮合成、17β-HSD3和3β-HSD1 mRNA表达的影响。方法:雄性SD大鼠19只,随机分为正常对照(NC)组10只,糖尿病(DM)组9只。DM组予高脂饮食加小剂量(25mg/kg)链脲佐菌素(STZ)诱导2型糖尿病大鼠模型,12周后处死。用光镜及电镜观察大鼠睾丸的组织形态学改变;RT-PCR法检测睾丸组织17β-羟基类固醇脱氢酶Ⅲ型(17β-HSD3)和3β-羟基类固醇脱氢酶Ⅰ型(3β-HSD1)mRNA含量;酶联免疫吸附法测定血清中睾酮含量。结果:糖尿病大鼠光镜下主要表现为睾丸曲细精管生精细胞数量减少及生精阻滞,Leydig细胞缩小,细胞核皱缩;透射电镜下主要见到Leydig细胞萎缩,线粒体、内质网等细胞器空泡样变及扩张,细胞核皱缩,染色质聚集;睾丸组织的17β-HSD3和3β-HSD1 mRNA含量和血清中睾酮含量糖尿病组均低于正常对照组。结论:糖尿病可使大鼠睾丸Leydig细胞变性,睾酮合成降低,其机制可能与降低17β-HSD3和3β-HSD1 mRNA表达有关。
Objective： To study the major pathological change of testis, the change of testosterone synthesis function of interstitial cell （Leydig cell） and the expression of 17 β-HSD3 mRNA and 3 β-HSD1 mRNA in diabetic rat. Methods： Nineteen male Sprague-Dauley rats were divided randomly into two groups： normal control group and diabetic group. The diabetic group was fed with high-fat diet and injected with strepozotocin intraperitoneally to induce type 2 diabetes mellitus. Twelve weeks later, the rats were sacrificed. The morphologic change of testicular tissue was observed under light microscopy （LM） and transmission electron microscopy （TEM）, respectively. The mRNA expression level of 17 β-hydroxysteroid dehydrogenase type 3 （17 β-HSDa） and 3 βhydroxysteroid dehydrogenase type 1 （3 β-HSDI） of testicular tissue were detected by RT-PCR, the serum testosterone （T） concentration was measured by ELISA. Results： The number of spermatogenic cell in seminiferous tubule was decreased and germinal arrest. Under IN, the Leydig cells were diminished and the nuclear was shrinked in diabetic group. Ultrastructural analysis of Leydig cells by TEM showed dilatation of the endoplasmic reticulum and mitochondrial swelling, and the chromatin was highly condensed in diabetic group. The mRNA levels of 17 β-HSD3 and 3 β-HSD1 of testicular tissue and the serom testosterone concentrations decreased in diabetic group compared with normal control group, Conclusion： Diabetes can cause morphologic change of Leydig ceils and decrease T production. The decreasing mRNA expression of 17 β-HSDa and 3 β-HSD1 may be involved in it.
出处
《温州医学院学报》
CAS
2008年第5期452-455,共4页
Journal of Wenzhou Medical College
基金
浙江省科技计划资助项目(2007C34003)
