Cerebral ischaemia/reperfusion injury could be managed by using tramadol

Basit Öğe Kaydı
dc.contributor.authorAkkurt, Ibrahim
dc.contributor.authorCetin, Cansel
dc.contributor.authorErdogan, Ahmet Melih
dc.contributor.authorDincel, Gungor Cagdas
dc.contributor.authorCeylan, Asli Fahriye
dc.contributor.authorKisa, Ucler
dc.contributor.authorBakar, Bulent
dc.date.accessioned2020-06-25T18:29:55Z
dc.date.available2020-06-25T18:29:55Z
dc.date.issued2018
dc.departmentKırıkkale Üniversitesi
dc.descriptionKISA, Ucler/0000-0002-8131-6810; DINCEL, Gungor Cagdas/0000-0002-6985-3197; BAKAR, BULENT/0000-0002-6236-7647
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.en_US
dc.identifier.citationclosedAccessen_US
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.scopus2-s2.0-85047351200
dc.identifier.scopusqualityQ3
dc.identifier.startpage774en_US
dc.identifier.urihttps://doi.org/10.1080/01616412.2018.1477556
dc.identifier.urihttps://hdl.handle.net/20.500.12587/7499
dc.identifier.volume40en_US
dc.identifier.wosWOS:000445794000009
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofNeurological Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAnti-inflammatoryen_US
dc.subjectapoptosisen_US
dc.subjectautophagyen_US
dc.subjectcerebral ischaemia/reperfusion injuryen_US
dc.subjecttramadolen_US
dc.titleCerebral ischaemia/reperfusion injury could be managed by using tramadolen_US
dc.typeArticle

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
[ X ]
İsim:
Cerebral ischaemia reperfusion injury could be managed by using tramadol.pdf
Boyut:
2.3 MB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin/Full Text
İndir

Koleksiyon

WOS İndeksli Yayınlar Koleksiyonu
Makale Koleksiyonu
Makale Koleksiyonu
PubMed İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu