A new perspective for the role of octadecaneuropeptide ODN in neurodegenerative diseases

Abstract

Event Abstract Back to Event A new perspective for the role of octadecaneuropeptide ODN in neurodegenerative diseases Olfa Masmoudi-Kouki1*, Yosra Hamdi1, Hadhemi Kaddour1, David Vaudry2, 3, Faouzi Jenhani4, Jerome Leprince2, 3, Marie-Christine Tonon2, 3 and Mohamed Amri1 1 Faculty of Science of Tunis, University Tunis El Manar, Laboratory of Functional Neurophysiology and Pathology, 00/UR/08-01, Department of Biological Sciences, Faculty of Science of Tunis, Tunisia 2 Inserm U413-EA4310, Inserm U413-EA4310, France 3 Laboratory of Neuronal and Neuroendocrine Communication and differentiation, European Institute for Peptide Research (IFRMP 23), Regional Platform for Cell Imaging of Haute-Normandie (PRIMACEN) , France 4 National Centre of Blood Transfusion, El Manar II 2092, Laboratory of Cellular Immunology and Cytometry, Tunisia Oxidative stress, resulting from accumulation of reactive oxygen species, plays a critical role on astroglial cell death associated with neurodegenerative diseases and stroke. Astroglial cells synthesize and release endozepines, a family of biologically active peptides that have been implicated in cellular protection. Thus, the purpose of the present study was to investigate the potential protective effect of one of the endozepines, the octadecaneuropeptide ODN, on H2O2-induced oxidative stress and cell death in rat astrocytes. Incubation of cultured astrocytes with graded concentrations of H2O2 for 1 h provoked a dose-dependent reduction of the number of living cells as evaluated by flow cytometric analysis and lactate dehydrogenase assay. The cytotoxic effect of H2O2 was associated with morphological modifications that are characteristic of apoptotic cell death. H2O2-treated cells exhibited high level of reactive oxygen species associated with a reduction of both superoxide dismutases (SOD) and catalase antioxidant enzymatic activities. Pre-treatment of astrocytes with very low concentrations of ODN (0.01 pM – 0.1 nM), dose-dependently prevented cell death induced by H2O2, and the effect of ODN was accompanied by a marked attenuation of ROS accumulation. ODN stimulated SOD and catalase activities in a concentration-dependent manner, and blocked H2O2-evoked inhibition of SOD and catalase activities. In addition, ODN totally suppressed H2O2-induced reduction of mitochondrial membrane potential. Taken together, these data demonstrate for the first time that the endozepine ODN is a potent protective agent that prevents oxidative stress-induced apoptotic cell death. Endozepines are thus potential candidates for development into therapeutically valuable agents for the treatment of cerebral injuries. Keywords: Apoptosis, Astrocytes, Catalase, Superoxide Dismutase Conference: 3rd Mediterranean Conference of Neuroscience , Alexandria, Egypt, 13 Dec - 16 Dec, 2009. Presentation Type: Poster Presentation Topic: CNS Diseases Citation: Masmoudi-Kouki O, Hamdi Y, Kaddour H, Vaudry D, Jenhani F, Leprince J, Tonon M and Amri M (2009). A new perspective for the role of octadecaneuropeptide ODN in neurodegenerative diseases. Front. Neurosci. Conference Abstract: 3rd Mediterranean Conference of Neuroscience . doi: 10.3389/conf.neuro.01.2009.16.156 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 25 Nov 2009; Published Online: 25 Nov 2009. * Correspondence: Olfa Masmoudi-Kouki, Faculty of Science of Tunis, University Tunis El Manar, Laboratory of Functional Neurophysiology and Pathology, 00/UR/08-01, Department of Biological Sciences, Faculty of Science of Tunis, 2092 Tunis, Tunisia, olfa.masmoudi@fst.utm.tn Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Olfa Masmoudi-Kouki Yosra Hamdi Hadhemi Kaddour David Vaudry Faouzi Jenhani Jerome Leprince Marie-Christine Tonon Mohamed Amri Google Olfa Masmoudi-Kouki Yosra Hamdi Hadhemi Kaddour David Vaudry Faouzi Jenhani Jerome Leprince Marie-Christine Tonon Mohamed Amri Google Scholar Olfa Masmoudi-Kouki Yosra Hamdi Hadhemi Kaddour David Vaudry Faouzi Jenhani Jerome Leprince Marie-Christine Tonon Mohamed Amri PubMed Olfa Masmoudi-Kouki Yosra Hamdi Hadhemi Kaddour David Vaudry Faouzi Jenhani Jerome Leprince Marie-Christine Tonon Mohamed Amri Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.