The effects of carvacrol on oxidative stress parameters and adoptosis process via TRPA1 channels in neuroblastoma cells

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dc.contributor.authorGünal, Mehmet Yalçın
dc.contributor.authorÖvey, İshak Suat
dc.date.accessioned2021-02-19T21:16:30Z
dc.date.available2021-02-19T21:16:30Z
dc.date.issued2019
dc.departmentALKÜ
dc.descriptionGunal, Mehmet/0000-0001-7702-2441
dc.description.abstractObjectives: This study is a preliminary study to investigate the effects of carvacrol (CRV) obtained from thyme on the apoptosis process in neuroblastoma cells. Methods: In this study, seven groups were designed as control, CRV, CRV + AP-18, CRV + melatonin, CRV + melatonin + AP-18, melatonin and melatonin + AP-18. All groups were stimulated using CNM (cinnamaldehyde) which is TRPA1 channel stimulator. Levels of Reactive oxygen species (ROS), caspase-3, caspase-9, mitochondrial depolarization, apoptosis, intracellular free calcium and 3-(4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide (MTT) were measured. Data were evaluated using one way ANOVA analysis. Results: Levels of ROS, mitochondrial depolarisation, caspase-3 and -9 and apoptosis were significantly higher in all groups treated with CRV compared to control (p < 0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, ROS and caspase-3 were significantly lower than control (p < 0.05). MTT levels were significantly decreased in all groups treated with CRV compared to control (p < 0.05). On the other hand, in melatonin-treated group and melatonin + AP-18 treated group, MTT was higher than control (p < 0.05). Conclusion: It has also been shown that CRV can also exert its effects through TRPA1 channels in neuroblastoma cells, which may accelerate the apoptosis process by acting on these channels, increasing ROS and caspase-3 levels. Changes in MTT levels support this result. However, in order to better evaluate the effects of CRV on the apoptosis process, it would be useful to investigate changes in caspase-9, mitochondrial depolarization, and calcium channels.
dc.identifier.doi10.32383/appdr/103422
dc.identifier.endpage542en_US
dc.identifier.issn0001-6837
dc.identifier.issn2353-5288
dc.identifier.issue3en_US
dc.identifier.scopusqualityQ4
dc.identifier.startpage535en_US
dc.identifier.urihttps://doi.org/10.32383/appdr/103422
dc.identifier.urihttps://hdl.handle.net/20.500.12868/457
dc.identifier.volume76en_US
dc.identifier.wosWOS:000473227700014
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.institutionauthor0-belirlenecek
dc.language.isoen
dc.publisherPolskie Towarzystwo Farmaceutyczne
dc.relation.ispartofActa Poloniae Pharmaceutica
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectapoptosis
dc.subjectcaspase-3
dc.subjectROS
dc.subjectneuroblastoma
dc.subjectcarvacrol
dc.titleThe effects of carvacrol on oxidative stress parameters and adoptosis process via TRPA1 channels in neuroblastoma cells
dc.typeArticle

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