Beta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse model

Basit Öğe Kaydı
dc.authoridKaya, Kürsat/0000-0002-6353-7791
dc.authoridbasak, nese/0000-0001-5566-8321
dc.authoridTaslidere, Elif/0000-0003-1723-2556
dc.authorwosidKaya, Kürsat/ABG-2848-2020
dc.authorwosidbasak, nese/ABH-5495-2020
dc.authorwosidTaslidere, Elif/ABI-8046-2020
dc.contributor.authorKaya, Kursat
dc.contributor.authorCiftci, Osman
dc.contributor.authorOztanir, Mustafa Namik
dc.contributor.authorTaslidere, Elif
dc.contributor.authorTurkmen, Nese Basak
dc.date.accessioned2024-08-04T20:46:53Z
dc.date.available2024-08-04T20:46:53Z
dc.date.issued2019
dc.departmentİnönü Üniversitesien_US
dc.description.abstractBeta-glucans (beta g), that have many useful effects on human health, are natural polysaccharides. Our aim in this study was to determine useful effect of beta g against oxidative and neuronal damage caused by global cerebral ischemia/reperfusion (IR) in stroke imitated mice via surgical operation. A total of 40 mice divided into four equal groups randomly. The group 1 (sham operated) was kept as control. Bilateral carotid arteries of subjects in group 2 (I/R) and group 4 (I/R + beta g) were clipped for 15 min, and the mice in group 4 (I/R + beta g) were treated with beta g (50 mg/kg/day), while the mice in group 2 (I/R) were treated with only vehicle for 10 days. The mice of group 3 (beta g) were treated with beta g for 10 days without carotid occlusion. Global cerebral I/R significantly increased oxidative stress and decreased members of anti-oxidant defense system. In addition, I/R caused histopathological damage in the brain tissue. However, beta g treatment ameliorated both oxidative and histopathological effects of I/R. Our present study showed that beta g treatment significantly ameliorated oxidative and histological damage in the brain tissue caused by cerebral I/R. Therefore, beta g treatment can be used as supportive care for ischemic stroke patients.en_US
dc.identifier.doi10.1590/s2175-97902019000218312
dc.identifier.issn1984-8250
dc.identifier.issn2175-9790
dc.identifier.scopus2-s2.0-85074269923en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1590/s2175-97902019000218312
dc.identifier.urihttps://hdl.handle.net/11616/99006
dc.identifier.volume55en_US
dc.identifier.wosWOS:000494326400001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherUniv Sao Paulo, Conjunto Quimicasen_US
dc.relation.ispartofBrazilian Journal of Pharmaceutical Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectGlobal cerebral I/Ren_US
dc.subjectOxidative stressen_US
dc.subjectNeuronal damageen_US
dc.subjectBeta-glucanen_US
dc.subjectC57BL/J6 miceen_US
dc.titleBeta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse modelen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu