Resveratrol attenuates hypoxia-induced neuronal cell death, inflammation and mitochondrial oxidative stress by modulation of TRPM2 channel

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dc.authoridNAZIROGLU, Mustafa/0000-0003-0887-6974
dc.authoridakyuva, yener/0000-0001-8171-5929
dc.contributor.authorAkyuva, Yener
dc.contributor.authorNaziroglu, Mustafa
dc.date.accessioned2024-09-18T21:03:17Z
dc.date.available2024-09-18T21:03:17Z
dc.date.issued2020
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractHypoxia (HYPX) induced-overload Ca2+ entry results in increase of mitochondrial oxidative stress, inflammation and apoptosis in several neurons. Ca2+ permeable TRPM2 channel was gated by ADPribose (ADPR) and reactive oxygen species (ROS), although its activity was modulated in HYPX-exposed neurons by resveratrol (RSV). The aim of this study was to evaluate if a therapy of RSV can modulate the effect of HYPX in the TRPM2 expressing SH-SY5Y neuronal and HEK293 (no expression of TRPM2) cell lines. The SH-SY5Y and HEK293 cells were divided into four groups as control, RSV (50 mu M and 24 hours), and HYPX and RSV + HYPX. For induction of HYPX in the cells, CoCl2 (200 mu M and 24 hours) incubation was used. HYPX-induced intracellular Ca2+ responses to TRPM2 activation were increased in the SH-SY5Y cells but not in the HEK293 cells from coming H2O2 and ADPR. RSV treatment improved intracellular Ca2+ responses, mitochondrial function, suppressed the generation of cytokine (IL-1 beta and TNF-alpha), cytosolic and mitochondrial ROS in the SH-SY5Y cells. Intracellular free Zn2+, apoptosis, cell death, PARP-1, TRPM2 expression, caspase -3 and -9 levels are increased through activating TRPM2 in the SH-SY5Y cells exposed to the HYPX. However, the values were decreased in the cells by RSV and TRPM2 blockers (ACA and 2-APB). In SH-SY5Y neuronal cells exposed to HYPX conditions, the neuroprotective effects of RSV were shown to be exerted via modulation of oxidative stress, inflammation, apoptosis and death through modulation of TRPM2 channel. RSV could be used as an effective agent in the treatment of neurodegeneration exposure to HYPX.en_US
dc.description.sponsorshipBSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, Industry and Trade Limited Company, Goller Bolgesi Teknokenti, Isparta, Turkey [2018-20]en_US
dc.description.sponsorshipThe authors declare no competing interests with respect to the research, financial, authorship, and/or publication of this article. This study was carried out with financial support from BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture, Industry and Trade Limited Company, Goller Bolgesi Teknokenti, Isparta, Turkey (Project No: 2018-20).en_US
dc.identifier.doi10.1038/s41598-020-63577-5
dc.identifier.issn2045-2322
dc.identifier.issue1en_US
dc.identifier.pmid32296107en_US
dc.identifier.scopus2-s2.0-85083479310en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1038/s41598-020-63577-5
dc.identifier.urihttps://hdl.handle.net/20.500.12483/13336
dc.identifier.volume10en_US
dc.identifier.wosWOS:000608593000001en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherNature Portfolioen_US
dc.relation.ispartofScientific Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDorsal-Root Ganglionen_US
dc.subjectCalcium-Ionen_US
dc.subjectAdp-Riboseen_US
dc.subjectInduced Neurotoxicityen_US
dc.subjectCa2+ Influxen_US
dc.subjectApoptosisen_US
dc.subjectDepletionen_US
dc.subjectTrpa1en_US
dc.subjectHippocampusen_US
dc.subjectInvolvementen_US
dc.titleResveratrol attenuates hypoxia-induced neuronal cell death, inflammation and mitochondrial oxidative stress by modulation of TRPM2 channelen_US
dc.typeArticleen_US

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