摘要
目的:观察糖尿病大鼠阴茎海绵体线粒体氧化应激损伤变化和还原型谷胱甘肽(reduced glutathione,GSH)对其氧化损伤的影响,探讨阴茎海绵体氧化应激的保护机制以及氧化应激在糖尿病勃起功能障碍发病机制中的作用。方法:成年雄性SD大鼠42只,随机取32只予以腹腔注射大剂量链脲佐菌素(streptozotocin,STZ),建成糖尿病大鼠模型25只,随机分为糖尿病组(n=13)、还原型谷胱甘肽治疗组(n=12),另10只设为正常对照组;饲养8周后用电刺激各组大鼠勃起神经测定海绵体内压评价勃起功能;采用黄嘌呤氧化酶法检测阴茎海绵体组织中超氧化物氧化酶(superoxide dismutase,SOD)活性,硫代巴比妥酸法测丙二醛(malondialdehyde,MDA)含量;光镜下观察Masson染色切片;Emaus法检测线粒体膜电位。结果:糖尿病组较正常对照组,阴茎海绵体MDA含量显著增高[(6.15±1.07)vs.(3.52±0.94)nmol/mg蛋白,P<0.01],SOD活性显著下降[(73.34±6.56)vs.(114.22±6.34)U/mg蛋白,P<0.05],海绵体内压(intracavernous pressure,ICP)峰值显著降低[(50.80±9.80)vs.(90.42±7.02)mmHg,P<0.05];GSH可使海绵体MDA含量明显降低[(3.90±0.96)vs.(6.15±1.07)nmol/mg蛋白,P<0.05],显著提高其SOD值[(95.74±4.65)vs.(73.34±6.56)U/mg蛋白,P<0.05]及ICP值[(74.20±5.69)vs.(50.80±9.80)mmHg,P<0.05]。糖尿病组大鼠阴茎组织中细胞线粒体膜电位减低[(727.98±68.33)vs.(1 223.15±222.92),P<0.01],而GSH则能提高线粒体膜电位[(930.30±48.36)vs.(727.98±68.33),P<0.05]。结论:糖尿病大鼠阴茎海绵体存在氧化应激损伤,抗氧化治疗起着保护阴茎组织细胞线粒体功能的作用,从而减轻勃起组织的氧化应激损伤,提高勃起能力;氧化应激在糖尿病性勃起功能障碍发病过程中起到了重要作用。
Objective： To explore the mechanism of impairment and defense of oxidative stress in ca-vernous 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 cavernous 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 cavernous tissue of diabetic rats and this impairment could contribute to diabetic erectile dysfunction;Oxidant treatment could attenuate oxidative stress by improving the function of mitochondria in cavernous tissue.Oxidative stress plays an important role in diabetic erectile dysfunction（DED） and our study might provide a new insight into the prevention and treatment of DED.
出处
《北京大学学报（医学版）》
CAS
CSCD
北大核心
2011年第2期189-193,共5页
Journal of Peking University:Health Sciences
基金
国家自然科学基金(30801143)资助~~
关键词
糖尿病
氧化性应激
线粒体
谷胱甘肽
勃起功能障碍
Oxidative stress； Mitochondria； Glutathione； Diabetes mellitus； Erectile dysfunction
