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

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dc.authoridTaşlidere, Aslı Cetin/0000-0003-3902-3210
dc.authoridAkyuva, Yener/0000-0001-8171-5929
dc.authoriddurak, mehmet akif akif/0000-0003-0827-2708
dc.authoridbasak, nese/0000-0001-5566-8321
dc.authoridCiftci, Osman/0000-0001-5755-3560
dc.authorwosidTaşlidere, Aslı Cetin/AAB-3979-2021
dc.authorwosidAkyuva, Yener/AAV-5706-2020
dc.authorwosiddurak, mehmet akif akif/ABI-1169-2020
dc.authorwosidbasak, nese/ABH-5495-2020
dc.contributor.authorOztanir, M. Namik
dc.contributor.authorCiftci, Osman
dc.contributor.authorCetin, Asli
dc.contributor.authorDurak, M. Akif
dc.contributor.authorBasak, Nese
dc.contributor.authorAkyuva, Yener
dc.date.accessioned2024-08-04T20:39:49Z
dc.date.available2024-08-04T20:39:49Z
dc.date.issued2014
dc.departmentİnönü Üniversitesien_US
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.en_US
dc.description.sponsorshipIUBAP (Scientific Research Fund of Inonu University) [2013/205]en_US
dc.description.sponsorshipWe acknowledge the support of IUBAP (Scientific Research Fund of Inonu University) under Grant 2013/205.en_US
dc.identifier.doi10.1007/s10072-014-1685-9
dc.identifier.endpage1228en_US
dc.identifier.issn1590-1874
dc.identifier.issn1590-3478
dc.identifier.issue8en_US
dc.identifier.pmid24554419en_US
dc.identifier.scopus2-s2.0-84905105839en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1221en_US
dc.identifier.urihttps://doi.org/10.1007/s10072-014-1685-9
dc.identifier.urihttps://hdl.handle.net/11616/96524
dc.identifier.volume35en_US
dc.identifier.wosWOS:000339964200010en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer-Verlag Italia Srlen_US
dc.relation.ispartofNeurological Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGlobal cerebral I/Ren_US
dc.subjectOxidative stressen_US
dc.subjectNeuronal damageen_US
dc.subjectGlycyrrhetinic aciden_US
dc.subjectC57BL/J6 miceen_US
dc.titleThe beneficial effects of 18?-glycyrrhetinic acid following oxidative and neuronal damage in brain tissue caused by global cerebral ischemia/reperfusion in a C57BL/J6 mouse modelen_US
dc.typeArticleen_US

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