BACKGROUND Oxidative stress has the potential to induce impotence, especially in diabetic patients. Peroxisome proliferator-activated receptor alpha (PPAR-α) agonists can potentiate antioxidants in a wide variety of tissues. However, no available evidence exists showing a direct antioxidant effect on testicular tissue in the setting of diabetes. Therefore, the aim of this study was to evaluate whether PPAR-α agonists can act directly to protect testicular tissue from oxidative damage. METHODS Male Wistar rats (180-200 g) were randomly allocated into four groups: normal control (N), normal treated (NF), diabetic (D), and diabetic treated (DF) (n = 6 for each group). Diabetes was induced by a single intravenous injection of streptozotocin STZ (40 mg/kg). Two treatment groups (diabetic and nondiabetic) were treated with fenofibrate daily for 8 weeks (80 mg/kg orally). At the end of 8 weeks, the animals were sacrificed and blood and testicular tissue samples collected. Nitrate, malondialdehyde, and glutathione levels, and the activity of superoxide dismutase and catalase enzymes were evaluated. The data were analyzed via two-way analysis of variance (ANOVA), with P < 0.05 taken as significant. RESULTS Diabetes significantly augmented free radicals, as attested by an increase in nitrate levels in testicular tissue, reduced activity of superoxide dismutase and catalase enzymes, and enhanced malondialdehyde content. These changes lead to oxidative stress in testicular tissues. Treatment with fenofibrate in the diabetic group improved oxidative stress by potentiation of antioxidant elements and a reduction in nitrate and malondialdehyde production. CONCLUSION Diabetes has a potent effect in promoting the development of oxidative damage in testicular tissue. The PPAR-a agonist fenofibrate improves the redox state and may prevent oxidative stress in the setting of diabetes-induced oxidative stress.

中文翻译：

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PPAR-α 激动剂非诺贝特改善糖尿病大鼠睾丸组织的氧化应激。

背景氧化应激具有诱发阳痿的潜力，尤其是在糖尿病患者中。过氧化物酶体增殖物激活受体 α (PPAR-α) 激动剂可以增强多种组织中的抗氧化剂。然而，没有可用的证据表明糖尿病患者对睾丸组织有直接的抗氧化作用。因此，本研究的目的是评估 PPAR-α 激动剂是否可以直接保护睾丸组织免受氧化损伤。方法 雄性 Wistar 大鼠（180-200 g）随机分为四组：正常对照（N）、正常治疗（NF）、糖尿病（D）和糖尿病治疗（DF）（每组 n = 6）。通过单次静脉注射链脲佐菌素 STZ (40 mg/kg) 诱发糖尿病。两个治疗组（糖尿病和非糖尿病）每天用非诺贝特治疗 8 周（口服 80 mg/kg）。在8周结束时，处死动物并收集血液和睾丸组织样品。评估了硝酸盐、丙二醛和谷胱甘肽水平，以及超氧化物歧化酶和过氧化氢酶的活性。数据通过双向方差分析（ANOVA）进行分析，P < 0.05 视为显着。结果 糖尿病会显着增加自由基，这可以通过睾丸组织中硝酸盐水平的增加、超氧化物歧化酶和过氧化氢酶的活性降低以及丙二醛含量增加来证明。这些变化导致睾丸组织中的氧化应激。在糖尿病组中用非诺贝特治疗通过增强抗氧化元素和减少硝酸盐和丙二醛的产生来改善氧化应激。结论 糖尿病具有促进睾丸组织氧化损伤发展的有效作用。PPAR-a 激动剂非诺贝特可改善氧化还原状态，并可能在糖尿病诱导的氧化应激环境中预防氧化应激。