北京大学学报（医学版）2011，Vol.43Issue(2)：189-193,5.DOI:10.3969/j.issn.1671-167X.2011.02.006
糖尿病大鼠阴茎海绵体线粒体氧化应激损伤与保护
Mechanisms of oxidative stress-induced damage and its protection in cavernous mitochondria of diabetic rats
摘要
Abstract
Objective : To explore the mechanism of impairment and defense of oxidative stress in cavernous mitochondria of diabetic rats. Methods : Adult male SD rats( n =42)were randomly divided into normal control group ( n = 10 ) and experimental group ( n = 32). The diabetic model rats induced by streptozotocin were randomly divided into diabetes group( n = 13 ) and therapeutic group with reduced glutathione ( GSH) treatment( n = 12) . Eight weeks later, erectile function was assessed by measuring the rise in intracavernous pressure ( ICP) of the rats following cavernous nerve eletrostimulation before the rats were sacrificed. The levels of malondialdehyde ( MDA) and the activities of superoxide dismutase ( SOD) in cavernous tissue were detected. The masson staining was used to show the structure of the rat penis. Mitochondrial transmembrane potential was detected. Results : A significant decrease in ICP was recorded in the diabetic rats [ (50. 80 ±9. 80) vs. ( 90. 42 ±7. 02 ) mmHg,P ＜ 0. 05 ] , with improvement measured in the rats receiving GSH[ (74. 20 ±5. 69 ) vs. (50. 80 ±9. 80) mmHg,P ＜0. 05 ] . The levels of MDA increased remarkably [ (6. 15 ± 1. 07 ) vs. ( 3. 52 ±0. 94 ) mmol/g protein , P ＜ 0. 01 ] and the activities of SOD decreased significantly [ (73. 34 ±6. 56) vs. ( 114. 22 ±6. 34 ) U/mg protein,P ＜ 0. 05 ) ] in cavernous tissue of the diabetes group. Mitochondria transmembrane potential was decreased [ (727.98 ±68. 33) vs. ( 1223. 15 ± 222. 92 ), P ＜ 0. 01 ]. A remarkable decrease in MDA [ (3. 90 ±0. 96 ) vs. (6. 15 ± 1. 07 ) mmol/g protein,P ＜0. 05 ] and increase in SOD [ (95. 74 ±4. 65 ) vs. (73. 34 ±6. 56 ) U/mg protein,P ＜ 0. 05 ] were observed in GSH treatment group. Meanwhile. the morphology changes of cavemous tissue and the decrease of mitochondria transmembrane potential were inhibited [ (930. 30 ±48. 36 ) vs. ( 727. 98 ± 68. 33 ) ,P ＜ 0. 05 ] , in diabetic rats with GSH treatment. Conclusion: Hyperglycemia could cause oxidative stress in the cavemous tissue of diabetic rats and this impairment couldcontribute to diabetic erectile dysfunction; Oxidant treatment could attenuate oxidative stress by improving the function of mitochondria in cavemous tissue. Oxidative stress plays an important role in diabetic erectile dysfunction ( DED) and our study might provide a new msight into the prevention and treatment of DED.关键词
糖尿病/氧化性应激/线粒体/谷胱甘肽/勃起功能障碍分类
医药卫生引用本文复制引用
李小鑫,邱雪峰,余文,朱伟东,陈赟 ,戴玉田..糖尿病大鼠阴茎海绵体线粒体氧化应激损伤与保护[J].北京大学学报（医学版）,2011,43(2):189-193,5.基金项目
国家自然科学基金(30801143)资助 （30801143）
