Morphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampus

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dc.authoridYILDIZHAN, Kenan/0000-0002-6585-4010
dc.authoridNAZIROGLU, Mustafa/0000-0003-0887-6974
dc.authoridakyuva, yener/0000-0001-8171-5929
dc.contributor.authorOsmanloglu, Omer
dc.contributor.authorYldirim, Mustafa Kemal
dc.contributor.authorAkyuva, Yener
dc.contributor.authorYildizhan, Kenan
dc.contributor.authorNaziroglu, Mustafa
dc.date.accessioned2024-09-18T20:02:34Z
dc.date.available2024-09-18T20:02:34Z
dc.date.issued2020
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractMorphine as an opioid is an important drug in the treatment of moderate to severe pain. Several stress factors via generation of nitric oxide (NO) and oxidative stress (OS) are responsible for the adverse effects of morphine-induced analgesia, addiction, and antinociceptive tolerance, including altered Ca(2+)concentration, inflammation, OS, and release of apoptotic factors. TRPM2 is a Ca2+-permeable cation channel and it is activated by OS and NO. Hence, adverse effect of morphine addiction may occur via the OS and NO-induced TRPM2 activation. Because of the unclear etiology of morphine-induced adverse effects in the hippocampus, investigating the involvement of TRPM2 and NO synthetase (NOS) activations in the treatment of morphine-induced OS, apoptosis, and neuroinflammation is a major challenge. The hippocampal neuron of TRPM2 wild-type (TRPM2-WT) and knockout (TRPM2-KO) mice were divided into control, morphine, NOS inhibitor (L-NAME) + morphine, and TRPM2 channel blockers (ACA and 2-APB) + morphine. The morphine-induced increases of apoptosis, neuron death, OS, lipid peroxidation, caspase-3 and caspase-9, neuroinflammatory cytokines (IL-1 beta, TNF-alpha, IL-6), and Ca(2+)levels in the hippocampal neuron of TRPM2-WT mouse were decreased by the L-NAME, ACA, and 2-APB treatments, although cell viability, neuron count, and reduced glutathione and glutathione peroxidase levels were increased by the treatments. However, the effects of morphine were not observed in the hippocampus of TRPM2-KO mice. Taken together, our data show that neurodegeneration adverse effects of morphine were induced by activation of TRPM2, and excessive generations of NO and OS. Thus, inhibition of TRPM2 may modulate morphine-induced neurodegeneration in the hippocampus.en_US
dc.description.sponsorshipBSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture and Industry Ltd., Isparta, Turkey [2018-033]en_US
dc.description.sponsorshipThe study was supported by BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture and Industry Ltd., Isparta, Turkey (Project No. 2018-033). Coordinator of the project wasM.N. There is no financial disclosure of the current study.en_US
dc.identifier.doi10.1007/s12035-020-01975-6
dc.identifier.endpage3389en_US
dc.identifier.issn0893-7648
dc.identifier.issn1559-1182
dc.identifier.issue8en_US
dc.identifier.pmid32524520en_US
dc.identifier.scopus2-s2.0-85087435259en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage3376en_US
dc.identifier.urihttps://doi.org/10.1007/s12035-020-01975-6
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7877
dc.identifier.volume57en_US
dc.identifier.wosWOS:000539512000002en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Neurobiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectNitric oxideen_US
dc.subjectMitochondriaen_US
dc.subjectMorphineen_US
dc.subjectTRPM2 channelen_US
dc.titleMorphine Induces Apoptosis, Inflammation, and Mitochondrial Oxidative Stress via Activation of TRPM2 Channel and Nitric Oxide Signaling Pathways in the Hippocampusen_US
dc.typeArticleen_US

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