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Antiapoptotic and Anti-Inflammatory Effects of Pparγ Agonist, Pioglitazone, Reversed Dox-Induced Cardiotoxicity Through Mediating of Mir-130A Downregulation in C57bl/6 Mice Publisher Pubmed



Pakravan G1 ; Peymani M2 ; Abedpoor N1, 3 ; Safaeinejad Z3 ; Yadegari M4 ; Derakhshan M5 ; Nasr Esfahani MH3 ; Ghaedi K1
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Authors Affiliations
  1. 1. Department of Cellular and Molecular Biology and Microbiology, Faculty of Biological Science and Technology, University of Isfahan, Isfahan, Iran
  2. 2. Department of Biology, Faculty of Basic Sciences, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
  3. 3. Department of Animal Biotechnology, Cell Science Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, Iran
  4. 4. Department of Diagnostic Imaging, Faculty of Veterinary Medicine, Shahrekord Branch, Islamic Azad University, Shahrekord, Iran
  5. 5. Department of Pathology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

Source: Journal of Biochemical and Molecular Toxicology Published:2022


Abstract

Doxorubicin (Dox) is an antitumor agent widely used in cancer therapy, with notable side effects of cardiac toxicity. Peroxisome proliferator-activated receptor γ (PPARγ), is a transcriptional factor with antiapoptotic and anti-inflammatory properties. Recently we indicated that cardiac toxicity of Dox was due to upregulation of miR-130a and further suppressive effect on cardiac Pparγ in vitro. In this study, we extended our proposed hypothesis in vivo. To achieve this, pioglitazone (Pio) and GW9662 were used as the specific agonist and antagonist of Pparγ to treat Dox-injected mice. Heart function, apoptosis, and inflammation in heart tissue were studied. Pretreatment of Dox-injected mice with Pio resulted in elevated expression of Pparγ and suppression of miR-130a. However, GW9662 pretreatment was unable to increase miR-130a expression. Pio pretreatment led to partially cardiac toxicity limitation of Dox whereas GW9662 caused heart damage. Finally, our observation determined that activation of Pparγ was not adequate to reverse the Dox-induced toxicity completely. © 2022 Wiley Periodicals LLC.
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