Protective Effects of Intralipid and Caffeic Acid Phenyl Esther (CAPE) on Neurotoxicity Induced by Ethanol in Rats

dc.authoridKorkmaz, Murat/0000-0002-4289-6541
dc.contributor.authorBasarslan, Seyit Kagan
dc.contributor.authorOsun, Arif
dc.contributor.authorSenol, Serkan
dc.contributor.authorKorkmaz, Murat
dc.contributor.authorOzkan, Umit
dc.contributor.authorKaplan, Ibrahim
dc.date.accessioned2024-09-18T20:19:53Z
dc.date.available2024-09-18T20:19:53Z
dc.date.issued2017
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractAIM: Ethanol causes oxidative degradation of the mitochondria! genome in the brain. This effect could contribute to the development of brain injury in some alcoholic patients. We investigated the protective effect of caffeic acid phenyl esther (CAPE) and intralipid (IL) on oxidative stress and neurotoxicity induced by ethanol intake. MATERIAL and METHODS: The forty-eight rats were randomly divided into seven groups. Ethanol was administered for acute toxicity. IL and CAPE were administered immediately after ethanol intake. Total oxidant status (TOS), total antioxidant status (TAS), and oxidative status index (OSi) were evaluated and histologic examination of cerebellum and brain tissue with Hematoxylin-Eosin and immuno-histochemical dyes was performed. RESULTS: In the ethanol group, TAS levels were significantly lower than the other groups and this finding indicates that the toxic effect of ethanol reduces antioxidant levels. In the ethanol group, TOS levels were significantly higher than the other groups. These results showed that ethanol induced oxidative stress. IL treatment increased TAS levels, and CAPE decreased TOS levels against ethanol toxicity. There was correlation between TAS and TOS levels. Also, histopathologic results confirmed these biochemical results. CONCLUSION: CAPE and IL treatment could be effective course of therapy to enhance therapeutic efficacy and may provide a promising approach for the treatment of neurotoxicity and oxidative stress induced by ethanol in clinic.en_US
dc.identifier.doi10.5137/1019-5149.JTN.14463-15.2
dc.identifier.endpage73en_US
dc.identifier.issn1019-5149
dc.identifier.issue1en_US
dc.identifier.pmid27593743en_US
dc.identifier.scopus2-s2.0-85009508776en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage66en_US
dc.identifier.urihttps://doi.org/10.5137/1019-5149.JTN.14463-15.2
dc.identifier.urihttps://hdl.handle.net/20.500.12483/9931
dc.identifier.volume27en_US
dc.identifier.wosWOS:000392042000009en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTurkish Neurosurgical Socen_US
dc.relation.ispartofTurkish Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectEthanolen_US
dc.subjectCaffeic acid phenyl esteren_US
dc.subjectIntralipiden_US
dc.subjectNeurotoxicityen_US
dc.titleProtective Effects of Intralipid and Caffeic Acid Phenyl Esther (CAPE) on Neurotoxicity Induced by Ethanol in Ratsen_US
dc.typeArticleen_US

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