Neuroprotective Effects of ?-Myrcene Following Global Cerebral Ischemia/Reperfusion-Mediated Oxidative and Neuronal Damage in a C57BL/J6 Mouse

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dc.authoridTaşlidere, Aslı Cetin/0000-0003-3902-3210
dc.authoridCiftci, Osman/0000-0001-5755-3560
dc.authorwosidTaşlidere, Aslı Cetin/AAB-3979-2021
dc.contributor.authorCiftci, Osman
dc.contributor.authorOztanir, M. Namik
dc.contributor.authorCetin, Asli
dc.date.accessioned2024-08-04T20:41:08Z
dc.date.available2024-08-04T20:41:08Z
dc.date.issued2014
dc.departmentİnönü Üniversitesien_US
dc.description.abstractThe aim of this study was to investigate the effects of beta-myrcene (MYR) on oxidative and histological damage in brain tissue caused by global cerebral ischemia/reperfusion (I/R) in C57BL/J6 mice. Mice (n = 40) were equally divided into four groups: (1) sham-operated (SH), (2) global cerebral I/R, (3) MYR, and (4) MYR + I/R. The SH group was used as a control and received 0.1 % carboxymethyl cellulose (CMC) as a vehicle following a medial incision without carotid occlusion. In the I/R group, the bilateral carotid arteries were clipped for 15 min, and treated with the vehicle intraperitoneally (i.p.) for 10 days. In the MYR group, mice were given 200 mg/kg MYR dissolved in 0.1 % CMC for 10 days following a medial incision without carotid occlusion. In the MYR + I/R group, the I/R procedure was performed exactly as in the I/R group, and they were then treated with the same dose of MYR for 10 days. Cerebral I/R induced oxidative stress via an increase in thiobarbituric acid reactive substances (TBARS) formation and a decrease in the antioxidant defense systems, including glutathione (GSH), catalase, glutathione peroxidase (GPx) and superoxide dismutase (SOD). However, MYR treatment protected against the oxidative effects of I/R by inducing significant increases in GSH, GPx, and SOD and a significant decrease in the formation of TBARS. Additionally, cerebral I/R increased the incidence of histopathological damage and apoptosis in brain tissue, but these neurodegenerative effects were eliminated by MYR treatment. This study has demonstrated that MYR effectively attenuates oxidative and histological damage in the brain caused by global I/R. The beneficial effects of MYR probably contribute to its strong antioxidant and radical scavenging properties. In conclusion, MYR may be useful for the attenuation of the negative effects of global cerebral I/R and, in the future, 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/s11064-014-1365-4
dc.identifier.endpage1723en_US
dc.identifier.issn0364-3190
dc.identifier.issn1573-6903
dc.identifier.issue9en_US
dc.identifier.pmid24972849en_US
dc.identifier.scopus2-s2.0-84939893272en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage1717en_US
dc.identifier.urihttps://doi.org/10.1007/s11064-014-1365-4
dc.identifier.urihttps://hdl.handle.net/11616/96940
dc.identifier.volume39en_US
dc.identifier.wosWOS:000341711800011en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer/Plenum Publishersen_US
dc.relation.ispartofNeurochemical Researchen_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.subjectbeta-Myrceneen_US
dc.subjectC57BL/J6en_US
dc.titleNeuroprotective Effects of ?-Myrcene Following Global Cerebral Ischemia/Reperfusion-Mediated Oxidative and Neuronal Damage in a C57BL/J6 Mouseen_US
dc.typeArticleen_US

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