Potential neuroprotective effect of gamma-glutamylcysteine ethyl ester on rat brain against kainic acid-induced excitotoxicity
dc.contributor.author | Yalcin, Ayfer | |
dc.contributor.author | Armagan, Guliz | |
dc.contributor.author | Turunc, Ezgi | |
dc.contributor.author | Konyalioglu, Sibel | |
dc.contributor.author | Kanit, Lutfiye | |
dc.date.accessioned | 2019-10-27T21:17:54Z | |
dc.date.available | 2019-10-27T21:17:54Z | |
dc.date.issued | 2010 | |
dc.department | Ege Üniversitesi | en_US |
dc.description.abstract | The aim of this study was to investigate the effect of gamma-Glutamylcysteine Ethyl Ester (GCEE) on the levels of GSH, caspase-3 activity, DNA damage and the expressions of Bcl-2, Bax and p53 mRNAs in rat hippocampus after status epilepticus (SE) induced by systemic kainic acid (KA). The male rats were divided into four groups as controls, KA (10 mg/kg), GCEE (10 mg/kg) and KA+GCEE. Glutathione (GSH) levels and caspase-3 activity were determined spectrophotometrically and colourimetrically, respectively. DNA damage and Bcl-2, Bax and p53 mRNA expressions were quantified by comet assay and reverse transcription followed by RT-PCR, respectively. KA treatment significantly depleted GSH levels, induced DNA damage, caspase-3 activity and the expressions of p53 and Bax mRNA. GCEE treatment protected GSH levels, decreased DNA damage and the levels of p53 and Bax/Bcl-2 mRNA against KA injection. These results indicate that GCEE treatment at the dose of 10 mg/kg is capable to protect the depleted levels of GSH and shows an anti-apoptotic activity due to the decreased levels of apoptotic biomarkers in the rat hippocampus after SE induced by KA. | en_US |
dc.description.sponsorship | Technological and Scientific Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [SBAG-K69-104S280] | en_US |
dc.description.sponsorship | This study was supported by the Technological and Scientific Council of Turkey (TUBITAK) (SBAG-K69-104S280 to A.Y). G. A and E. T were also supported by doctoral grants from TUBITAK. The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. | en_US |
dc.identifier.doi | 10.3109/10715761003645964 | en_US |
dc.identifier.endpage | 521 | en_US |
dc.identifier.issn | 1071-5762 | |
dc.identifier.issn | 1029-2470 | |
dc.identifier.issue | 5 | en_US |
dc.identifier.pmid | 20214503 | en_US |
dc.identifier.startpage | 513 | en_US |
dc.identifier.uri | https://doi.org/10.3109/10715761003645964 | |
dc.identifier.uri | https://hdl.handle.net/11454/43889 | |
dc.identifier.volume | 44 | en_US |
dc.identifier.wos | WOS:000276815300004 | en_US |
dc.identifier.wosquality | Q2 | en_US |
dc.indekslendigikaynak | Web of Science | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.language.iso | en | en_US |
dc.publisher | Taylor & Francis Ltd | en_US |
dc.relation.ispartof | Free Radical Research | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.title | Potential neuroprotective effect of gamma-glutamylcysteine ethyl ester on rat brain against kainic acid-induced excitotoxicity | en_US |
dc.type | Article | en_US |