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Cerium and Yttrium Oxide Nanoparticles and Nano-Selenium Produce Protective Effects Against H2o2-Induced Oxidative Stress in Pancreatic Beta Cells by Modulating Mitochondrial Dysfunction Publisher Pubmed



Tavoosi S1 ; Baghsheikhi AH1 ; Shetabboushehri SV2, 3 ; Navaeinigjeh M4 ; Sarvestani NN5 ; Karimi MY3 ; Ranjbar A6 ; Ebadollahinatanzi A7 ; Hosseini A3
Authors
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Authors Affiliations
  1. 1. Department of Biology, East Tehran Branch, Islamic Azad University, Tehran, Iran
  2. 2. Department of Toxicology & Pharmacology, School of Pharmacy, International Campus, Iran University of Medical Sciences, Tehran, Iran
  3. 3. Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran
  4. 4. Pharmaceutical Sciences Research Center, The Institute of Pharmaceutical Sciences (TIPS), Tehran University of Medical Science, Tehran, Iran
  5. 5. Department of Animal Biology, School of Biology, Department of Science, University of Tehran, Tehran, Iran
  6. 6. Nutrition Health Research Center, Hamadan University of Medical Sciences, Hamadan, Iran
  7. 7. Medicinal plants Department, Imam Khomeini Higher Education Center, Agricultural Research, Education and Extension Organization (AREEO), Karaj, Iran

Source: Pharmaceutical Nanotechnology Published:2020


Abstract

Background: Type 1 diabetes mellitus is characterized by the destruction of in-sulin-producing Beta cells in the pancreas. Researchers hope that islet transplantation will help to patients with insulin-dependent diabetes mellitus (IDDM). Oxidative stress is the most important challenge that beta cells face to it after isolation, and mitochondrial dysfunction is a crucial mediator in beta cells death. Hence, therapeutic approaches can shift to antioxidants through the application of nanoparticles such as cerium and yttrium oxide nanoparticles (Cer and Ytt Ox NPs) and nano-selenium (Nan Se). Objective: This study evaluates the effects of Cer and Ytt Ox NPs and Nan Se on H2O2-induced oxidative stress in pancreatic beta cells with focus on mitochondrial dysfunction pathway. Methods: CRI-D2 beta-cell line were pretreated with Cer Ox NPs (200 µM) + Ytt Ox NPs (0.5 µg/mL) for 3 days and/or Nan Se (0.01 µM) for 1 day. Then markers of oxidative stress, mitochondrial dysfunction, insulin and glucagon secretion were measured. Results: We reported a decrease in H2O2-induced reactive oxygen species (ROS) level and glucagon secretion, and an increase in H2O2-reduced ATP/ADP ratio, MMP, as well as UCP2 protein expression, and insulin secretion by pretreatment of CRI-D2 cells with Cer and Ytt Ox NPs and/or Nan Se. Conclusion: We found maximum protective effect with Cer and Ytt Ox NPs on CRI-D2 beta-cell line exposed by H2O2 for keeping beta cells alive until transplant whereas combination of Cer and Ytt Ox NPs and Nan Se had very little protective effect in this condition. © 2020 Bentham Science Publishers.
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