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Critical Reviews™ in Eukaryotic Gene Expression

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ISSN Imprimer: 1045-4403

ISSN En ligne: 2162-6502

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PPAR-α Agonist Fenofibrate Ameliorates Oxidative Stress in Testicular Tissue of Diabetic Rats

Volume 30, Numéro 2, 2020, pp. 93-100
DOI: 10.1615/CritRevEukaryotGeneExpr.2020027918
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RÉSUMÉ

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.

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CITÉ PAR
  1. Chakkarwar VishalArvind, Kawtikwar Pravin, Fenofibrate prevents nicotine-induced acute kidney injury: Possible involvement of endothelial nitric oxide synthase, Indian Journal of Nephrology, 31, 5, 2021. Crossref

  2. Muzio Giuliana, Barrera Giuseppina, Pizzimenti Stefania, Peroxisome Proliferator-Activated Receptors (PPARs) and Oxidative Stress in Physiological Conditions and in Cancer, Antioxidants, 10, 11, 2021. Crossref

  3. Feng Junxia, Lu Meizhi, Li Wenhao, Li Jingchun, Meng Ping, Li Zukai, Gao Xuejuan, Zhang Yunfang, PPARγ alleviates peritoneal fibrosis progression along with promoting GLUT1 expression and suppressing peritoneal mesothelial cell proliferation, Molecular and Cellular Biochemistry, 477, 7, 2022. Crossref

  4. Saidi Azeezat O., Akintayo Christopher O., Atuma Chukwubueze L., Mahmud Hadiza, Sabinari Isaiah W., Oniyide Adesola A., Aturamu Ayodeji, Agunbiade Toluwani B., Olaniyi Kehinde S., Melatonin supplementation preserves testicular function by attenuating lactate production and oxidative stress in high fat diet-induced obese rat model, Theriogenology, 187, 2022. Crossref

  5. Mahmoudi Ali, Moallem Seyed Adel, Johnston Thomas P., Sahebkar Amirhossein, Mandard Stéphane, Liver Protective Effect of Fenofibrate in NASH/NAFLD Animal Models, PPAR Research, 2022, 2022. Crossref

  6. Mahmoudi Ali, Jamialahmadi Tannaz, Johnston Thomas P., Sahebkar Amirhossein, Impact of fenofibrate on NAFLD/NASH: A genetic perspective, Drug Discovery Today, 27, 8, 2022. Crossref

  7. Warzecha Karolina W., Pudełek Maciej, Catapano Jessica, Madeja Zbigniew, Czyż Jarosław, Long-Term Fenofibrate Treatment Stimulates the Phenotypic Microevolution of Prostate Cancer Cells In Vitro, Pharmaceuticals, 15, 11, 2022. Crossref

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