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Comparative Clinical Pathology

, Volume 28, Issue 1, pp 203–209 | Cite as

PPAR-α agonist fenofibrate potentiates antioxidative elements and improves oxidative stress of hepatic cells in streptozotocin-induced diabetic animals

  • Habib YaribeygiEmail author
  • Mohammad Taghi Mohammadi
  • Alexandra E. Butler
  • Amirhossein SahebkarEmail author
Original Article
  • 25 Downloads

Abstract

Oxidative stress induced by hyperglycemia has a crucial role in hepatocellular disorders. The aim of this study was to evaluate whether fenofibrate potentiates the anti-oxidant defense system of hepatocytes and thereby prevents oxidative stress. Male Wistar rats were assigned to four groups: normal control (C), normal-treated (CF), diabetic (D), and diabetic-treated (DF) (n = 6 per group). Hyperglycemia was induced with streptozotocin (single dose of 45 mg/kg into the tail vein). Treated groups received fenofibrate for 8 weeks by intragastric gavage (80 mg/kg/day). At study completion (day 56), the rats were sacrificed and liver tissue harvested. Catalase (CAT) and superoxide dismutase (SOD) enzymes activities, malondialdehyde (MDA), nitrate, and glutathione (GLT) contents were evaluated in all experimental groups. Obtained data were analyzed via two-way ANOVA, p < 0.05 taken as significant. Hyperglycemia markedly decreased SOD and CAT enzyme activities; furthermore, oxidative stress was induced via MDA content enhancement. Fenofibrate increased both SOD and CAT enzyme activities and decreased the nitrate content and MDA production in hepatic cells, thus improving oxidative stress. Our data suggest that uncontrolled hyperglycemia overwhelms the anti-oxidant defense systems of hepatic cells and oxidative damage ensues. The PPAR-α agonist Fenofibrate prevents oxidative damage in hepatocytes by potentiating the anti-oxidant defense system and can therefore improve the redox state in hepatocellular tissue.

Keywords

Oxidative stress Liver PPAR-α Fenofibrate Malondialdehyde 

Notes

Acknowledgements

This study was carried out by a grant from the School of Medicine of the Baqiyatallah University of Medical Sciences. We wish to thank the Department of Physiology and Biophysics and the Deputy of Research of the Medical School of Baqiyatallah University and also the Clinical Research Development Center of the Baqiyatallah Hospital for providing technical support.

Funding

This study was financially supported by the Baqiyatallah University of Medical Sciences, Tehran, Iran.

Compliance with ethical standards

This manuscript complies with the ethical standards of Comparative Clinical Pathology.

Conflict of interest

The authors declare that they have no conflicts of interest.

Ethical approval and informed consent

All protocols of the study were approved by the Ethics Committee of the Baqiyatallah University of Medical Sciences. Informed consent was not applicable for this animal study.

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Copyright information

© Springer-Verlag London Ltd., part of Springer Nature 2018

Authors and Affiliations

  1. 1.Chronic Kidney Disease Research CenterShahid Beheshti University of Medical SciencesTehranIran
  2. 2.Department of Physiology and Biophysics, School of MedicineBaqiyatallah University of Medical SciencesTehranIran
  3. 3.Life Sciences Research DivisionAnti-Doping Laboratory QatarDohaQatar
  4. 4.Neurogenic Inflammation Research CenterMashhad University of Medical SciencesMashhadIran
  5. 5.Biotechnology Research Center, Pharmaceutical Technology InstituteMashhad University of Medical SciencesMashhadIran
  6. 6.School of PharmacyMashhad University of Medical SciencesMashhadIran

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