A different view on the platelet aggregation inhibitor clopidogrel - a well-suitable anti-oedema agent in a preclinical model of brain injury?

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dc.contributor.authorGünal, Mehmet Yalçın
dc.contributor.authorYuluğ, Burak
dc.contributor.authorÇağlayan, Berrak
dc.contributor.authorOzansoy, Mehmet
dc.contributor.authorKılıç, Ülkan
dc.contributor.authorKeskin, İlknur
dc.contributor.authorKılıç, Ertuğrul
dc.date.accessioned2021-02-19T21:16:50Z
dc.date.available2021-02-19T21:16:50Z
dc.date.issued2019
dc.departmentALKÜ, Fakülteler, Sağlık Bilimleri Fakültesi, Fizyoterapi ve Rehabilitasyon Bölümü
dc.descriptionGünal, Mehmet/0000-0001-7702-2441
dc.description.abstractAim: The neuroprotective effects of clopidogrel have already been shown in various experimental models. Taking into account the fact that clopidogrel is well tolerated and approved for use in various clinical settings, it can be an attractive candidate for further clinical investigations, especially when the anti-oedema effect appears to be a reasonable adjuvant strategy, such as in brain injury (BI). Here we aimed to examine the neuroprotective role of clopidogrel in BI. Methods: To investigate the effects of clopidogrel, we induced BI in mice using a cold trauma model and evaluated the underlying cell survival/death mechanisms via cresyl violet, TUNEL staining and western blot analysis. Results: Clopidogrel at a dose of 3 mg/kg led to a significant reduction in brain swelling. Similar decreases were observed with 10 mg/kg and 30 mg/kg of clopidogrel. We also have shown that clopidogrel blocks the prominent inflammatory injury pathways and exerts a significant anti-apoptotic effect (3 and 30 mg/kg), which has boon associated with increased neuronal cell survival pathways. Clopidogrel (3, 10 and 30 mg/kg) dose-dependently altered the JNK, p-38, AKT, ERK and p53 levels. Conclusion: Our findings demonstrate that clopidogrel can be a novel candidate for the reduction of post-traumatic BI and oedema. We propose that it can be applied mainly in the acute phases of cerebral ischaemia, which is characterized by haemorrhagic transformation and brain oedema.
dc.identifier.doi10.14735/amcsnn2019526
dc.identifier.endpage532en_US
dc.identifier.issn1210-7859
dc.identifier.issn1802-4041
dc.identifier.issue5en_US
dc.identifier.scopusqualityQ3
dc.identifier.startpage526en_US
dc.identifier.urihttps://doi.org/10.14735/amcsnn2019526
dc.identifier.urihttps://hdl.handle.net/20.500.12868/563
dc.identifier.volume82en_US
dc.identifier.wosWOS:000500973400007
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.institutionauthorGünal, M. Yalçın
dc.language.isoen
dc.publisherCzech Medical Soc
dc.relation.ispartofCeska A Slovenska Neurologie A Neurochirurgie
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectclopidogrel
dc.subjectbrain injury
dc.subjectneuroprotective effect
dc.subjectbrain swelling
dc.subjectinfarct volume
dc.subjectcell survival pathways
dc.titleA different view on the platelet aggregation inhibitor clopidogrel - a well-suitable anti-oedema agent in a preclinical model of brain injury?
dc.typeArticle

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