Adıyaman Üniversitesi Kurumsal Arşivi

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

Basit öğe kaydını göster

dc.contributor.author Kaya, Kürsat
dc.contributor.author Çiftçi, Osman
dc.contributor.author ve öte.
dc.date.accessioned 2025-04-08T06:06:10Z
dc.date.available 2025-04-08T06:06:10Z
dc.date.issued 2019
dc.identifier.issn 1984-8250
dc.identifier.uri http://dspace.adiyaman.edu.tr:8080/xmlui/handle/20.500.12414/6056
dc.description.abstract Beta-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. tr
dc.language.iso en tr
dc.publisher UNIV SAO PAULO, tr
dc.subject Global cerebral I/R tr
dc.subject Oxidative stress tr
dc.subject Neuronal damage tr
dc.subject Beta-glucan tr
dc.subject C57BL/J6 mice tr
dc.title Beta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse model tr
dc.type Article tr
dc.contributor.authorID 0000-0002-6353-7791 tr
dc.contributor.department Adiyaman Univ, Fac Pharm, Dept Biochem, tr
dc.contributor.department Pamukkale Univ, Fac Med, Dept Med Pharmacol, tr
dc.identifier.volume 55 tr
dc.source.title BRAZILIAN JOURNAL OF PHARMACEUTICAL SCIENCES tr


Bu öğenin dosyaları:

Bu öğe aşağıdaki koleksiyon(lar)da görünmektedir.

Basit öğe kaydını göster