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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(SODEx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SODEX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),SODEx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SODEx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。
Objective To investigate the role of oxidative damage in the pathogenesis of diabetic ED and the intervention of reduced glutathione (GSH) on oxidative damage, and to provide a new method for clinical treatment. Methods Fifty adult male Sprague-Dawley rats were randomly divided into 4 groups: group A was control group (n = 10), group B was diabetes intervention group (n = 13), group C diabetes insulin intervention group ) And D group were diabetic insulin + GSH intervention group (n = 14). The model of diabetes was made by intraperitoneal injection of STZ and screened. After 8 weeks, the corpus cavernosum tissues of rats were homogenized, and the activity of superoxide dismutase (SOD) in corpus cavernosum tissues was determined by xanthine oxidation method. The content of malondialdehyde (MDA) PCR method to detect the expression of extracellular SOD gene (SODEx gene); Western-blot assay CuZnSOD protein content. Results The corpus cavernosum in group A basically had no accumulation of peroxidation products. Compared with group A, the activity of SOD in group B, C and D decreased significantly (P <0.05), the content of MDA increased significantly (P <0.05), the expression of SODEX gene in group B, C and D, and the content of CuZnSOD (P <0.05). Compared with group B, the activity of SOD in group C and group D was significantly increased (P <0.05), the content of MDA was significantly decreased (P <0.05), the expression of SODEx gene and the content of CuZnSOD protein were significantly increased (P <0.05). Compared with group C, SODEx gene expression and CuZnSOD protein content in group D were significantly increased (P <0.05). Conclusion The free radical metabolism of corpus cavernosum in diabetic male rats is obviously obstructed, the lipid peroxidation products increase and the oxygen free radical scavenging ability declines. However, the application of antioxidant GSH can partially reduce the oxidative damage. Prompted that oxidative damage may play a role in the development of diabetic ED. This study provides a new strategy for the prevention and treatment of diabetic ED.