Cyproheptadine causes apoptosis and decreases inflammation by disrupting thiol/disulfide balance and enhancing the levels of SIRT1 in C6 glioblastoma cells

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dc.authoridSAHINTURK, VAROL/0000-0003-2317-3644
dc.authorwosidkar, fatih/AAI-4540-2021
dc.authorwosidSAHINTURK, VAROL/V-5195-2017
dc.contributor.authorKacar, Sedat
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorKar, Fatih
dc.contributor.authorSahinturk, Varol
dc.contributor.authorKanbak, Gungor
dc.date.accessioned2021-12-01T18:48:10Z
dc.date.available2021-12-01T18:48:10Z
dc.date.issued2021
dc.department[Belirlenecek]en_US
dc.description.abstractCyproheptadine is first-generation antihistamine drug, that is, H1 receptor antagonist, with a drug being anesthetic, anti-serotonergic and anti-cholinergic and started to be used clinically in the 1960s. As firstly utilized as an anti-allergic drug, usage of cyproheptadine was expanded to other cases including serotonin syndrome, appetite increasing, migraines and insomnia. However, there are almost few studies seeking to explore the association between cyproheptadine and cancer in general. In the present study, we sought to determine the impact of cyproheptadine on C6 glioblastoma cells by morphological, biochemical and cytotoxic analyzes. We searched the effective doses of cyproheptadine for C6 glioblastoma cells and examined the cells under an inverted microscope. Next, we determined the protein levels of SIRT1, NF?B and IL-6 protein. Then, we measured and calculated the levels of thiols, disulfide bonds and related parameters. After that, we evaluated apoptotic activity by Annexin V and caspase 3 assays. As a result, we detected a dose-dependent increase in apoptosis and SIRT 1 protein levels, and a decrease in inflammatory proteins. Furthermore, we have detected a drop in thiol and disulfide content. Our study suggests that Cyproheptadine causes apoptosis and decreases inflammation by disrupting thiol/disulfide balance and enhancing the levels of SIRT1, offering the potential for being an anticancer drug. Therefore, it might be further investigated in future studies.en_US
dc.identifier.doi10.1016/j.tiv.2021.105135
dc.identifier.issn0887-2333
dc.identifier.issn1879-3177
dc.identifier.pmid33675893en_US
dc.identifier.scopus2-s2.0-85102116813en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1016/j.tiv.2021.105135
dc.identifier.urihttps://hdl.handle.net/20.500.12684/10471
dc.identifier.volume73en_US
dc.identifier.wosWOS:000643464000011en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherPergamon-Elsevier Science Ltden_US
dc.relation.ispartofToxicology In Vitroen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCyproheptadineen_US
dc.subjectGlioblastoma cellsen_US
dc.subjectThiolen_US
dc.subjectdisulfide balanceen_US
dc.subjectInflammationen_US
dc.subjectApoptosisen_US
dc.subjectCytotoxicityen_US
dc.subjectAnnexin Ven_US
dc.subjectHistamineen_US
dc.subjectGrowthen_US
dc.subjectAssayen_US
dc.titleCyproheptadine causes apoptosis and decreases inflammation by disrupting thiol/disulfide balance and enhancing the levels of SIRT1 in C6 glioblastoma cellsen_US
dc.typeArticleen_US

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