Neuroprotective effects of N-acetylcysteine on experimental closed head trauma in rats

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dc.authoridHicdonmez, Tufan/0000-0003-4847-8727
dc.authorwosidHicdonmez, Tufan/AGI-0165-2022
dc.contributor.authorHicdonmez, Tufan
dc.contributor.authorKanter, Mehmet
dc.contributor.authorTiryaki, Mehmet
dc.contributor.authorParsak, Turgay
dc.contributor.authorCobanoglu, Sebahattin
dc.date.accessioned2024-06-12T11:16:41Z
dc.date.available2024-06-12T11:16:41Z
dc.date.issued2006
dc.departmentTrakya Üniversitesien_US
dc.description.abstractN-acetylcysteine (NAC) is a precursor of glutathione, a potent antioxidant, and a free radical scavenger. The beneficial effect of NAC on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of NAC on nervous system trauma remains less understood. Therefore, we aimed to investigate the therapeutic efficacy of NAC with an experimental closed head trauma model in rats. Thirty-six adult male Sprague-Dawley rats were randomly divided into three groups of 12 rats each: Group I (control), Group II (trauma-alone), and Group III (trauma+NAC treatment). In Groups II and III, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 2 h (Subgroups I-A, II-A, and III-A) and 12 h (Subgroups I-B, II-B, and III-B) after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. The closed head trauma significantly increased tissue malondialdehyde (MDA) levels (P < 0.05), and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities (P < 0.05), but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of NAC (150 mg/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels (P < 0.05) and also significantly (P < 0.05) increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the trauma-alone group, the neurons became extensively dark and degenerated into picnotic nuclei. The morphology of neurons in the NAC treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+NAC treatment groups. In conclusion, the NAC treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications.en_US
dc.identifier.doi10.1007/s11064-006-9040-z
dc.identifier.endpage481en_US
dc.identifier.issn0364-3190
dc.identifier.issn1573-6903
dc.identifier.issue4en_US
dc.identifier.pmid16758355en_US
dc.identifier.scopus2-s2.0-33745035900en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage473en_US
dc.identifier.urihttps://doi.org/10.1007/s11064-006-9040-z
dc.identifier.urihttps://hdl.handle.net/20.500.14551/24392
dc.identifier.volume31en_US
dc.identifier.wosWOS:000238138800004en_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.subjectTraumaen_US
dc.subjectBrain Tissueen_US
dc.subjectMDAen_US
dc.subjectAntioxidant Enzyme Activityen_US
dc.subjectN-Acetylcysteineen_US
dc.subjectCaspase-3en_US
dc.subjectRaten_US
dc.subjectControlled Cortical Impacten_US
dc.subjectBrain-Injuryen_US
dc.subjectLipid-Peroxidationen_US
dc.subjectAcetyl-Cysteineen_US
dc.subjectOxidative Stressen_US
dc.subjectApoptosisen_US
dc.subjectIschemiaen_US
dc.subjectAntioxidantsen_US
dc.subjectSuperoxideen_US
dc.subjectActivationen_US
dc.titleNeuroprotective effects of N-acetylcysteine on experimental closed head trauma in ratsen_US
dc.typeArticleen_US

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