Therapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in rats

dc.authoridCEYLAN, TAYFUN/0000-0002-0917-0378
dc.authoridKarabulut, Derya/0000-0003-2067-6174
dc.authoridAKIN, Ali Tugrul/0000-0002-1408-8571
dc.authoridTASKIRAN, Mehmet/0000-0003-0061-6908
dc.authorwosidCEYLAN, TAYFUN/AAF-1001-2021
dc.authorwosidTAŞKIRAN, Mehmet/AAP-4414-2021
dc.authorwosidKarabulut, Derya/N-4942-2019
dc.contributor.authorCeylan, Tayfun
dc.contributor.authorAkin, Ali Tugrul
dc.contributor.authorKarabulut, Derya
dc.contributor.authorTan, Fazile Canturk
dc.contributor.authorTaskiran, Mehmet
dc.contributor.authorYakan, Birkan
dc.date.accessioned2024-05-19T14:39:05Z
dc.date.available2024-05-19T14:39:05Z
dc.date.issued2023
dc.departmentİstinye Üniversitesien_US
dc.description.abstractNonylphenol (NP), causes various harmful effects such as cognitive impairment and neurotoxicity. Thymoquinone (TQ), has antioxidant, anti-inflammatory, and neuroprotective properties. In this study, our aim is to investigate the effects of TQ on the brain damage caused by NP. Corn oil was applied to the control group. NP (100 mg/kg/day) was administered to the NP and NP + TQ groups for 21 days. TQ (5 mg/kg/day) was administered to the NP + TQ and TQ groups for 7 after 21 days. At the end of the experiment, the new object recognition test was applied to the rats and the rats were killed and their brain tissues were removed. Sections taken from brain tissues were stained with hematoxylin-eosin for histopathological evaluation. In addition, neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), Cas-3, and nerve growth factor (NGF) immunoreactivities were evaluated in brain tissue sections. In addition, malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) activities were determined. Comet assay was applied to determine DNA damage in cells. The results of our study showed that NP, caused behavioral disorders and damage to the cerebral cortex in rats. This damage in the form of neuron degeneration seen in the cortex was associated with apoptosis involving Cas-3 activation, increased DNA damage, and free oxygen radicals. NP, SOD, and CAT caused a decrease in enzyme activities. In addition, the cellular protein NeuN was decreased, astrocytosis-associated GFAP was increased, and growth factor NGF was decreased. When all our evaluations are taken together, treatment with TQ showed an ameliorative effect on the behavioral impairment and brain damage caused by NP exposure.en_US
dc.description.sponsorshipErciyes University Scientific Research Projects Unit [TDK-2020-10202]en_US
dc.description.sponsorshipACKNOWLEDGMENTS This study was supported by Erciyes University Scientific Research Projects Unit with the project code TDK-2020-10202.en_US
dc.identifier.doi10.1002/jbt.23471
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue11en_US
dc.identifier.pmid37466128en_US
dc.identifier.scopus2-s2.0-85165386071en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org10.1002/jbt.23471
dc.identifier.urihttps://hdl.handle.net/20.500.12713/4696
dc.identifier.volume37en_US
dc.identifier.wosWOS:001028700300001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Biochemical and Molecular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.snmz20240519_kaen_US
dc.subjectAntioxidanten_US
dc.subjectBehavioral Impairmenten_US
dc.subjectBrain Damageen_US
dc.subjectNonylphenolen_US
dc.subjectThymoquinoneen_US
dc.titleTherapeutic effect of thymoquinone on brain damage caused by nonylphenol exposure in ratsen_US
dc.typeArticleen_US

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