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dc.contributor.authorCetin, Cansel
dc.contributor.authorErdogan, Ahmet Melih
dc.contributor.authorDincel, Gungor Cagdas
dc.contributor.authorBakar, Bulent
dc.contributor.authorKisa, Ucler
dc.date.accessioned2020-06-25T18:23:04Z
dc.date.available2020-06-25T18:23:04Z
dc.date.issued2017
dc.identifier.citationclosedAccessen_US
dc.identifier.issn0188-4409
dc.identifier.issn1873-5487
dc.identifier.urihttps://doi.org/10.1016/j.arcmed.2017.06.004
dc.identifier.urihttps://hdl.handle.net/20.500.12587/7001
dc.descriptionDINCEL, Gungor Cagdas/0000-0002-6985-3197; KISA, Ucler/0000-0002-8131-6810en_US
dc.descriptionWOS: 000411909400004en_US
dc.descriptionPubMed: 28923326en_US
dc.description.abstractBackground. Management of cerebral ischemia/reperfusion (I/R) injury is still difficult process today. Aims of the Study. Aim of present study was to investigate therapeutic properties of sulfasalazine in cerebral transient I/R injury in rat. Methods. Except Control group (n = 5), 20 Wistar albino rats were allocated for acute and chronic stage investigation of I/R injury, and temporary aneurysm clips were attempted to both internal carotid arteries for thirty min. Four hours later, 40 mg/kg once a day sulfasalazine was administered to animals of SL-A and SL-C groups, orally. Animals were decapitated, following which pyknotic and necrotic neuronal cells, perivascular edema, irregularities of intercellular organization (IIO) of hippocampal regions, and cortical necrotic neurons of parietal lobe were counted or scaled histopathologically. Tissue malonyldialdehyde (MDA), myeloperoxidation (MPO), total nitrite/nitrate (NO), interleukin 1-beta (IL-1 beta), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) level values were evaluated biochemically. Results. Sulfasalazine could reduce perivascular edema, 110, cortical and hippocampal neuronal cell death in both stages. It could decrease MDA in acute stage, but not reduce IL-1 beta, IL-6, MPO, NO, and TNF alpha levels. It could increase IL-1 beta levels in chronic stage but not affect to IL-6, MPO, MDA, NO, TNF-alpha levels. Conclusion. Sulfasalazine could improve histopathological architecture of hypoxic tissue in both stages of FR injury in rat. It could inhibit lipid peroxidation cascades just in acute stage. These results suggested that therapeutic mechanisms of sulfasalazine in cerebral I/R injury should be investigated by using more specific laboratory methods in future studies. (C) 2017 IMSS. Published by Elsevier Inc.en_US
dc.language.isoengen_US
dc.publisherElsevier Science Incen_US
dc.relation.isversionof10.1016/j.arcmed.2017.06.004en_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAntiinflamatoryen_US
dc.subjectCerebral hypoxia reperfusion injuryen_US
dc.subjectSulfasalazineen_US
dc.subjectStrokeen_US
dc.titleEffects of Sulphasalazine in Cerebral Ischemia Reperfusion Injury in Raten_US
dc.typearticleen_US
dc.contributor.departmentKırıkkale Üniversitesien_US
dc.identifier.volume48en_US
dc.identifier.issue3en_US
dc.identifier.startpage247en_US
dc.identifier.endpage256en_US
dc.relation.journalArchives Of Medical Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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