Protective effect of 5-HT7 receptor activation against glutamate-induced neurotoxicity in human neuroblastoma SH-SY5Y cells via antioxidative and antiapoptotic pathways

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dc.authorid0000-0003-2042-5949
dc.authorid0000-0003-0836-7205
dc.authorid0000-0002-0659-3084
dc.authorscopusid55367802000
dc.authorscopusid55933545700
dc.authorscopusid6508093438
dc.authorscopusid16174252200
dc.authorscopusid26025725000
dc.authorscopusid56779839000
dc.authorwosidYUKSEL, Tugba Nurcan/ABA-6278-2020
dc.authorwosidPOLAT, Beyzagül/G-6010-2012
dc.authorwosidCADIRCI, ELIF/AAW-4534-2020
dc.contributor.authorYüksel, Tuğba Nurcan
dc.contributor.authorYayla, Muhammed
dc.contributor.authorHalıcı, Zekai
dc.contributor.authorÇadırcı, Elif
dc.contributor.authorPolat, Beyzagül
dc.contributor.authorKöse, Duygu
dc.date.accessioned2022-05-11T14:41:12Z
dc.date.available2022-05-11T14:41:12Z
dc.date.issued2019
dc.departmentFakülteler, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Tıbbi Farmakoloji Ana Bilim Dalı
dc.description.abstractSerotonin exerts anti-inflammatory, antioxidant and antiapoptotic effects through 5-HT7 receptors. The present study determined the role of 5-HT7 receptors in glutamate-induced neurotoxicity by using human SH-SY5Y neuroblastoma cells. The cells were pretreated with different concentrations of 5-HT7 receptor agonist LP44 and antagonist SB269970 for 60 min, followed by treatment with glutamate. Cell proliferation was measured using xCELLigence system. Treatment with all the concentrations of LP44 significantly protected the cells from the toxic effects of glutamate after 24, 48 and 72 h. Although 5-HT7 receptor expression was significantly upregulated in glutamate-treated cells, it was downregulated in LP44-pretreated cells. Furthermore, LP44 treatment significantly decreased malondialdehyde levels and increased superoxide dismutase activities and glutathione levels. Moreover, LP44 treatment significantly decreased tumor necrosis factor alpha (TNF-a) levels and inhibited caspase 3 and caspase 9 mRNA expression. In contrast, SB269970 treatment exerted an insignificant effect on oxidative stress, inflammation and apoptosis. These findings suggest that exogenous stimulation of the 54-1T7 receptors may be protective in glutamate-induced neurotoxicity and that 5-HT7 receptor agonists can be used as therapeutic agents for preventing glutamate-induced neurological disorders.
dc.description.sponsorshipTUBITAKTurkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [112S627]
dc.description.sponsorshipThis study is a part of Tugba Nurcan YUKSEL PhD thesis and is supported by TUBITAK (project number: 112S627). We would like to extend our special thanks to Yasin BAYIR and Abdulmecit ALBAYRAK for their contribution.
dc.identifier.doi10.1016/j.ntt.2019.01.002
dc.identifier.endpage28
dc.identifier.issn0892-0362
dc.identifier.issn1872-9738
dc.identifier.pmid30685503
dc.identifier.scopus2-s2.0-85060544693
dc.identifier.scopusqualityQ2
dc.identifier.startpage22
dc.identifier.urihttps://doi.org/10.1016/j.ntt.2019.01.002
dc.identifier.urihttps://hdl.handle.net/20.500.11776/9104
dc.identifier.volume72
dc.identifier.wosWOS:000463131300003
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorYüksel, Tuğba Nurcan
dc.language.isoen
dc.publisherPergamon-Elsevier Science Ltd
dc.relation.ispartofNeurotoxicology and Teratology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectGlutamate
dc.subjectSerotonin
dc.subject5-HT7
dc.subjectTNF-alpha
dc.subjectInduced Neuronal Death
dc.subjectOxidative Stress
dc.subjectMitochondrial Dysfunction
dc.subjectMediated Neurotoxicity
dc.subjectSerotonin
dc.subjectMechanisms
dc.subjectExpression
dc.subjectAgonist
dc.subjectNeuroprotection
dc.subjectSuperoxide
dc.titleProtective effect of 5-HT7 receptor activation against glutamate-induced neurotoxicity in human neuroblastoma SH-SY5Y cells via antioxidative and antiapoptotic pathways
dc.typeArticle

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