Objective To investigate the mechanism of oxidative damnification during the developement of diabetic erection dysfunction(DMED) and explore the effect of reduced glutathione on oxidative damnification. Methods Fifty male Sptague-Dawley rats were randomly divided into 4 groups including group A(control group, n=10), group B(no intervention diabetic group,n=13), C group(insulin intervention diabetic group, n=13) and D group(diabetic insulin and GSH intervention group,n=14). The diabetic model was established by the intraperitoneal injection of streptozotoc. Homogenates of corpus cavernosum tissue of rats was ready for next analysis. The thiobarbaturic acid (TBA) method was used to determine the lipid peroxidation, SOD activity was measured using the xanthine-oxidase cytochrome c method. The expression of SODex gene was detected by RT-PCR and level of CuZnSOD protein by Western-blot. Results There was almost no lipid peroxidation product detected in the corpus cavernosum tissue of the rats in group A. Compare with that of group A, SOD activity, the expression of SODex gene and CuZnSOD protein significantly decreased in B, C, D groups (P<0.05) whereas MDA level significantly increased(P<0.05). Compare with that of group B, SOD activity, the expression of SOD_(ex) gene and CuZnSOD protein in C, D groups significantly increased (P<0.05) whereas MDA level significantly decreased (P<0.05). Compare with that of C group, the expression of SOD_(ex) gene of D groups, and CuZnSOD protein significantly increased (P<0.05). Conclusion The metabolism was distinctly disturbed in the corpus cavernosum tissue of the diabetic male rats such as increase of the lipid peroxidation product and decrease of the free radical eliminating. Reduced GSH could reduced the oxidative damnification partly, which indicated that oxidative damnification might be involved in the development of DMED. Our study might provide a new insight for prevention and treatment of DMED.%目的 探讨氧化损伤在糖尿病性ED发病机制中的作用,以及还原型谷胱甘肽(GSH)对氧化损伤的干预作用,为临床治疗提供新的手段.方法 成年雄性SD大鼠50只,随机分为4组:A组为对照组(N=10),B组为糖尿病无干预组(N=13),C组为糖尿病胰岛素干预组(N=13)和D组为糖尿病胰岛素+GSH干预组(N=14).采用腹腔注射STZ法制作糖尿病模型并进行筛选.8周后取大鼠阴茎海绵体组织进行组织匀浆,采用黄嘌呤氧化法测定阴茎海绵体组织中超氧化物岐化酶(SOD)活性:用TBA法测定丙二醛(MDA)含量;RT-PCR法检测胞外型SOD基因(SOD_(EX)基因)的表达;WESTERN-BLOT法检测CUZNSOD蛋白含量.结果 A组大鼠海绵体组织基本无过氧化产物蓄积.与A组相比,B、C、D组的SOD活性显著下降(P<0.05),MDA含量均显著升高(P<0.05),B、C、D组SOD_(EX)基因的表达、CUZNSOD蛋白含量显著下降(P<0.05);与B组相比,C、D组的SOD活性显著升高(P<0.05),MDA含量显著下降(P<0.05),SOD_(EX)基因的表达及CUZNSOD蛋白含量显著升高(P<0.05).与C组相比,D组SOD_(EX)基因的表达及CUZNSOD蛋白含量显著升高(P<0.05).结论 糖尿病性雄性大鼠阴茎海绵体组织自由基代谢明显障碍,脂质过氧化产物增加,同时氧自由基清除能力下降;而抗氧化剂GSH的应用能部分减弱氧化损伤.提示氧化损伤可能在糖尿病性ED的发生发展中起一定作用.本研究为糖尿病性ED的预防和治疗提供新的策略.
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