| 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 |