Noopept Attenuates Diabetes-Mediated Neuropathic Pain and Oxidative Hippocampal Neurotoxicity via Inhibition of TRPV1 Channel in Rats

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dc.authoridGürbüz, Perihan/0000-0002-6632-9197
dc.authoridAKATLI, AYSE NUR/0000-0002-9677-2456
dc.authoridDUZOVA, Halil/0000-0001-8123-2150
dc.authoridNAZIROGLU, Mustafa/0000-0003-0887-6974
dc.authorwosidGürbüz, Perihan/Y-4833-2018
dc.authorwosidÇİĞ, BILAL/A-1747-2018
dc.authorwosidAKATLI, AYSE NUR/ABH-4455-2020
dc.contributor.authorDuzova, Halil
dc.contributor.authorNaziroglu, Mustafa
dc.contributor.authorCig, Bilal
dc.contributor.authorGurbuz, Perihan
dc.contributor.authorAkatli, Ayse Nur
dc.date.accessioned2024-08-04T20:50:24Z
dc.date.available2024-08-04T20:50:24Z
dc.date.issued2021
dc.departmentİnönü Üniversitesien_US
dc.description.abstractNeuropathic pain and oxidative neurotoxicity are two adverse main actions of diabetes mellitus (DM). The expression levels of calcium ion (Ca2+) permeable TRPV1 channels are high in the dorsal root ganglion (DRGs) and hippocampus (HIPPO). TRPV1 is activated by capsaicin and reactive free oxygen radicals (fROS) to mediate peripheral neuropathy and neurotoxicity. Noopept (NP) acted several protective antioxidant actions against oxidative neurotoxicity. As DM is known to increase the levels of fROS, the protective roles of antioxidant NP were evaluated on the DM-mediated neurotoxicity and neuropathic pain via the modulation of TRPV1 in rats. Thirty-six rats were equally divided into control, NP, DM (streptozotocin, STZ), and STZ + NP groups. A decrease on the STZ-mediated increase of neuropathic pain (via the analyses of Von Frey and hot plate) and blood glucose level was observed by the treatment of NP. A protective role of NP via downregulation of TRPV1 activity on the STZ-induced increase of apoptosis, mitochondrial fROS, lipid peroxidation, caspase -3 (CASP-3), caspase -9 (CASP-9), TRPV1 current density, glutathione (GSH), cytosolic free Zn2+, and Ca2+ concentrations in the DRGs and HIPPO was also observed. The STZ-mediated decrease of glutathione peroxidase, GSH, vitamin E, and beta-carotene concentrations in the brain cortex, erythrocyte, liver, kidney, and plasma was also attenuated by the treatment of NP. The STZ-mediated increase of TRPV1, CASP-3, and CASP-9 expressions was decreased in the DRGs and HIPPO by the treatment of NP. In conclusion, the treatment of NP induced protective effects against STZ-induced adverse peripheral pain and HIPPO oxidative neurotoxicity. These effects might attribute to the potent antioxidant property of NP.en_US
dc.description.sponsorshipInonu University, BAPSIS [TCD-2019-624]en_US
dc.description.sponsorshipThis research was supported by the Inonu University, BAPSIS (Project number: TCD-2019-624). Coordinator of the project was Dr. Duzova.en_US
dc.identifier.doi10.1007/s12035-021-02478-8
dc.identifier.endpage5051en_US
dc.identifier.issn0893-7648
dc.identifier.issn1559-1182
dc.identifier.issue10en_US
dc.identifier.pmid34241806en_US
dc.identifier.scopus2-s2.0-85110017300en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage5031en_US
dc.identifier.urihttps://doi.org/10.1007/s12035-021-02478-8
dc.identifier.urihttps://hdl.handle.net/11616/100038
dc.identifier.volume58en_US
dc.identifier.wosWOS:000672111700001en_US
dc.identifier.wosqualityQ2en_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.subjectDiabetesen_US
dc.subjectNeuropathic painen_US
dc.subjectNoopepten_US
dc.subjectOxidative stressen_US
dc.subjectTRPV1 channelen_US
dc.titleNoopept Attenuates Diabetes-Mediated Neuropathic Pain and Oxidative Hippocampal Neurotoxicity via Inhibition of TRPV1 Channel in Ratsen_US
dc.typeArticleen_US

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