Abstract

Event Abstract Back to Event Changes in Nitric Oxide Synthase (NOS), Cyclooxygenase-2 (COX-2) and Superoxide Dismutase (SOD) Protein Levels in Chronic Cerebral Hypoperfusion in Rats Eva Mracsko1*, Marietta Hugyecz1, Adam Institoris1, Eszter Farkas1 and Ferenc Bari1 1 Department of Physiology, Faculty of Medicine, University of Szeged, Hungary Chronic cerebral hypoperfusion is a mild ischemic condition associated with cognitive deficits. Its experimental model is the permanent occlusion of the common carotid arteries (2VO) in rats resulting in neuronal damage and microglia-activation. Several mechanisms including oxidative stress and glutamate toxicity have been reported to be involved in this pathway. Our purpose was to determine the changes in the expression of several prooxidant and antioxidant enzymes caused by hypoperfusion. Male Wistar rats were exposed to the 2VO (n=27) or SHAM operation (n=29). Alternatively, some rats not operated on (naive) (n=12). Tissue samples from the hippocampus and frontal cortex were taken 1 day, 3 days, 1 week, 3 - 6 - and 12 months following surgery. Western blot analysis was used to determine the expression of endothelial (e), inducible (i), neuronal (n) NOS, COX-2 and manganese SOD (MnSOD). The expression of COX-2 and eNOS enzymes increased at the early phase of hypoperfusion. These early changes were more profound in the hippocampus and can show the presence of neurotoxicity and vascular actions caused by ischemia. The expression of nNOS and iNOS enzymes was less meaningful at the early stage of hypoperfusion and there was no change in the MnSOD enzyme level. There was a significant reduction of most of the enzyme levels 3 months after 2VO, which can be the result of neuronal loss. One year of hypoperfusion showed an upregulation in eNOS expression which can strengthen the adaptation of the brain to cerebral ischemia. Supported by OTKA K63401 and IN69967. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - degenerative disorders Citation: Mracsko E, Hugyecz M, Institoris A, Farkas E and Bari F (2009). Changes in Nitric Oxide Synthase (NOS), Cyclooxygenase-2 (COX-2) and Superoxide Dismutase (SOD) Protein Levels in Chronic Cerebral Hypoperfusion in Rats. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.164 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: 05 Mar 2009; Published Online: 05 Mar 2009. * Correspondence: Eva Mracsko, Department of Physiology, Faculty of Medicine, University of Szeged, Szeged, Hungary, mracskoeva@gmail.com 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 Eva Mracsko Marietta Hugyecz Adam Institoris Eszter Farkas Ferenc Bari Google Eva Mracsko Marietta Hugyecz Adam Institoris Eszter Farkas Ferenc Bari Google Scholar Eva Mracsko Marietta Hugyecz Adam Institoris Eszter Farkas Ferenc Bari PubMed Eva Mracsko Marietta Hugyecz Adam Institoris Eszter Farkas Ferenc Bari 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.

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