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The beneficial effects of 18 beta-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model

dc.contributor.authorÖZTANIR, MUSTAFA NAMIK
dc.contributor.authorÇİFTÇİ, OSMAN
dc.contributor.authorCetin, Asli
dc.contributor.authorDURAK, MEHMET AKİF
dc.contributor.authorBasak, Nese
dc.contributor.authorAkyuva, Yener
dc.contributor.institutionauthorÖZTANIR, MUSTAFA NAMIK
dc.date.accessioned2021-01-27T20:59:22Z
dc.date.available2021-01-27T20:59:22Z
dc.date.issued2014-08-01T00:00:00Z
dc.description.abstractThis study investigated the effects of 18 beta-glycyrrhetinic acid (GA) on neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. All subjects (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) I/R, (3) GA, and (4) GA+I/R. The SH group was used as a control. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and the mice were treated with the vehicle for 10 days. In the GA group, mice were given GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the GA+I/R group, the I/R model was applied to the mice exactly as in the I/R group, and they were then treated with the same dose of GA for 10 days. Cerebral I/R significantly induced oxidative stress via an increase in lipid peroxidaitons and a decrease in elements of the antioxidant defense systems. However, GA treatment was protective against the oxidative effects of I/R by inducing significant increases in antioxidant defense systems and a significant decrease of lipid peroxidations. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by GA treatment. Therefore, the current study demonstrated that GA treatment effectively prevents oxidative and histological damage in the brain caused by global I/R. In this context, GA may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, it may be a viable and safe alternative treatment for ischemic stroke in humans.
dc.identifier.citationÖZTANIR M. N. , ÇİFTÇİ O., Cetin A., DURAK M. A. , Basak N., Akyuva Y., -The beneficial effects of 18 beta-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model-, NEUROLOGICAL SCIENCES, cilt.35, ss.1221-1228, 2014
dc.identifier.doi10.1007/s10072-014-1685-9
dc.identifier.scopus84905105839
dc.identifier.urihttp://hdl.handle.net/20.500.12645/28191
dc.identifier.wosWOS:000339964200010
dc.titleThe beneficial effects of 18 beta-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse model
dc.typeArticle
dspace.entity.typePublication
local.avesis.id9c85a2f7-65f3-4051-87e1-c40c7d281962
local.publication.isinternational1
relation.isAuthorOfPublicationae4f7327-851c-4ef2-94a7-789ed77869a8
relation.isAuthorOfPublication.latestForDiscoveryae4f7327-851c-4ef2-94a7-789ed77869a8
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