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Effect of Gallic Acid on PTZ-induced Neurotoxıcıty, Oxidative Stress and Inflammation in SH-SY5Y Neuroblastoma Cells

dc.contributor.authorYazğan, Yener
dc.date.accessioned2026-01-04T20:22:10Z
dc.date.issued2024-04-30
dc.description.abstractAim: Human neuroblastoma cell lines are widely used to elucidate the cellular and molecular mechanisms of neurotoxicants and to facilitate the prioritization of in vivo testing. Pentylenetetrazole (PTZ) is a tetrazole derivative. Although PTZ is the most commonly used chemical to create an in vivo and in vitro epilepsy (EP) model, its mechanism of action in neuronal cells has not been fully elucidated. Gallic acid (GA) has broad biological properties such as antioxidant, anti-microbial, and anti-inflammatory activities. This study aimed to investigate the effect of GA on PTZ-induced neurotoxicity in neuroblastoma cells. Methods: For the study, four groups were formed from SH-SY5Y neuroblastoma cells as control (C), GA (100 μM), PTZ (30 μM), and PTZ+GA. In the study, total antioxidant and oxidant status (TAS and TOS), inflammatory cytokines (TNF α, IL 1β, and IL 6), lipid peroxidation levels as malondialdehyde (MDA), glutathione peroxidase (GSHPx), and glutathione (GSH) levels in the SH-SY5Y neuroblastoma cells were determined. Results: The results showed that PTZ treatment caused neurotoxicity in the neuroblastoma cell line and increased TOS, TNF α, IL 1β, IL 6, and MDA levels while decreasing TAS, GSH, and GSHPx levels. This situation improved with GA treatment. Conclusion: As a result, it was determined that GA treatment showed a protective effect in the PTZ-induced neural toxicity model in SH-SY5Y human neuroblastoma cell lines.
dc.description.urihttps://doi.org/10.30565/medalanya.1415132
dc.description.urihttps://doaj.org/article/a16093fdfab7427caf5198ac6c48480e
dc.description.urihttps://dergipark.org.tr/tr/pub/medalanya/issue/84380/1415132
dc.identifier.doi10.30565/medalanya.1415132
dc.identifier.eissn2587-0319
dc.identifier.endpage12
dc.identifier.openairedoi_dedup___::9c096a078f69b97cc801aaa61a756828
dc.identifier.orcid0000-0002-5613-6906
dc.identifier.startpage8
dc.identifier.urihttps://hdl.handle.net/20.500.12597/41756
dc.identifier.volume8
dc.publisherActa Medica Alanya
dc.relation.ispartofActa Medica Alanya
dc.rightsOPEN
dc.subjectpentylenetetrazole
dc.subjectClinical Sciences (Other)
dc.subjectR
dc.subjectpentilenetetrazol
dc.subjectNeurotoxicity
dc.subjectSH-SY5Y neuroblastoma cell
dc.subjectGallic acid
dc.subjectPentylenetetrazole
dc.subjectsh-sy5y nöroblastom hücresi
dc.subjectNörotoksisite
dc.subjectSH-SY5Y nöroblastom hücresi
dc.subjectGallik asit
dc.subjectPentilenetetrazol
dc.subjectnörotoksisite
dc.subjectneurotoxicity
dc.subjectMedicine
dc.subjectgallik asit
dc.subjectgallic acid
dc.subjectKlinik Tıp Bilimleri (Diğer)
dc.subjectsh-sy5y neuroblastoma cell
dc.subject.sdg3. Good health
dc.titleEffect of Gallic Acid on PTZ-induced Neurotoxıcıty, Oxidative Stress and Inflammation in SH-SY5Y Neuroblastoma Cells
dc.typeArticle
dspace.entity.typePublication
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Pentylenetetrazole (PTZ) is a tetrazole derivative. Although PTZ is the most commonly used chemical to create an in vivo and in vitro epilepsy (EP) model, its mechanism of action in neuronal cells has not been fully elucidated. Gallic acid (GA) has broad biological properties such as antioxidant, anti-microbial, and anti-inflammatory activities. This study aimed to investigate the effect of GA on PTZ-induced neurotoxicity in neuroblastoma cells. Methods: For the study, four groups were formed from SH-SY5Y neuroblastoma cells as control (C), GA (100 μM), PTZ (30 μM), and PTZ+GA. In the study, total antioxidant and oxidant status (TAS and TOS), inflammatory cytokines (TNF α, IL 1β, and IL 6), lipid peroxidation levels as malondialdehyde (MDA), glutathione peroxidase (GSHPx), and glutathione (GSH) levels in the SH-SY5Y neuroblastoma cells were determined. Results: The results showed that PTZ treatment caused neurotoxicity in the neuroblastoma cell line and increased TOS, TNF α, IL 1β, IL 6, and MDA levels while decreasing TAS, GSH, and GSHPx levels. This situation improved with GA treatment. 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