Effects of sulphasalazine in cerebral ıschemia reperfusion ınjury in rat

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dc.authoridKISA, UCLER -- 0000-0002-8131-6810; DINCEL, Gungor Cagdas -- 0000-0002-6985-3197
dc.contributor.authorÇetin, Cansel
dc.contributor.authorErdoğan, Ahmet Melih
dc.contributor.authorDinçel, Güngör Cağdaş
dc.contributor.authorBakar, Bülent
dc.contributor.authorKısa, Üçler
dc.date.accessioned13.07.201910:50:10
dc.date.accessioned2019-07-29T19:28:16Z
dc.date.available13.07.201910:50:10
dc.date.available2019-07-29T19:28:16Z
dc.date.issued2017
dc.departmentEskil Meslek Yüksekokulu
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.
dc.identifier.doi10.1016/j.arcmed.2017.06.004
dc.identifier.endpage256en_US
dc.identifier.issn0188-4409
dc.identifier.issn1873-5487
dc.identifier.issue3en_US
dc.identifier.pmid28923326
dc.identifier.scopusqualityQ1
dc.identifier.startpage247en_US
dc.identifier.urihttps://doi.org/10.1016/j.arcmed.2017.06.004
dc.identifier.urihttps://hdl.handle.net/20.500.12451/6013
dc.identifier.volume48en_US
dc.identifier.wosWOS:000411909400004
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Science Inc
dc.relation.ispartofArchives of Medical Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAntiinflamatory
dc.subjectCerebral Hypoxia Reperfusion Injury
dc.subjectSulfasalazine
dc.subjectStroke
dc.titleEffects of sulphasalazine in cerebral ıschemia reperfusion ınjury in rat
dc.typeArticle

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