Cerebral ischaemia/reperfusion injury could be managed by using tramadol

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dc.authoridDINCEL, Gungor Cagdas -- 0000-0002-6985-3197; BAKAR, BULENT -- 0000-0002-6236-7647
dc.contributor.authorAkkurt, İbrahim
dc.contributor.authorÇetin, Cansel
dc.contributor.authorErdoğan, Ahmet Melih
dc.contributor.authorDinçel, Güngör Çağdaş
dc.contributor.authorCeylan, Aslı Fahriye
dc.contributor.authorKısa, Üçler
dc.contributor.authorOppong, Jonathan
dc.contributor.authorAkkurt, Adem
dc.contributor.authorÖgden, Mustafa
dc.contributor.authorBakar, Bülent
dc.date.accessioned13.07.201910:50:10
dc.date.accessioned2019-07-16T09:17:18Z
dc.date.available13.07.201910:50:10
dc.date.available2019-07-16T09:17:18Z
dc.date.issued2018
dc.departmentEskil Meslek Yüksekokulu
dc.description.abstractObjectives: No valid treatment modality that will repair stroke damage and provide neurological recovery has yet been identified in literature. Studies demonstrated that adequate quality of life could be provided if post-stroke pain could be treated sufficiently and timely. Besides its pain relief effects, tramadol has oedema-reducing and anti-inflammatory properties. With these in mind, this study investigated the influence of tramadol in acute and/or chronic ischaemia/reperfusion (I/R) injury. Methods: Putting aside the Control group, 23 Wistar albino rats were distributed to four groups to investigate the acute (Sham-A, TR-A) and chronic (Sham-C, TR-C) periods of I/R injury, and temporary aneurysm clips were applied to their internal carotid arteries for 30 min. Four hours after clippage, tramadol was administered to animals of TR-A and TR-C groups intraperitoneally. After sacrificing all animals, pyknotic and necrotic neuronal cells in hippocampal cornu ammonis (CA)1, CA2, CA3 and parietal cortical regions were counted, and perivascular oedema, intercellular organization disorder (IOD) and inflammatory cell infiltration were scaled histopathologically. Additionally, tissue interleukin (IL)-1 beta, IL-10, malondialdehyde, nitric oxide, tumour necrosis factor-alpha, caspase-3, beclin-1, Atg12, LC3II/LC3I levels were measured biochemically. Results: Tramadol could minimize perivascular oedema, IOD, parietal and hippocampal neuronal necrosis, inflammatory cell infiltration in both periods of I/R injury histopathologically. Apart from inhibiting apoptosis and enhancing autophagy, tramadol had no influence on any other biochemical result. Discussion: Tramadol can ameliorate the histopathological structure of ischaemic tissue in both periods of I/R injury in rat. We suggest further research investigating various dosages with different administration methods of tramadol in stroke should be conducted by adopting different explorative techniques.
dc.identifier.doi10.1080/01616412.2018.1477556
dc.identifier.endpage784en_US
dc.identifier.issn0161-6412
dc.identifier.issn1743-1328
dc.identifier.issue9en_US
dc.identifier.pmid29792388
dc.identifier.scopusqualityQ3
dc.identifier.startpage774en_US
dc.identifier.urihttps://doi.org/10.1080/01616412.2018.1477556
dc.identifier.urihttps://hdl.handle.net/20.500.12451/4730
dc.identifier.volume40en_US
dc.identifier.wosWOS:000445794000009
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis
dc.relation.ispartofNeurological Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectAnti-Inflammatory
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectCerebral Ischaemia/Reperfusion Injury
dc.subjectTramadol
dc.titleCerebral ischaemia/reperfusion injury could be managed by using tramadol
dc.typeArticle

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