Protective Effects of G Protein-Coupled Estrogen Receptor 1 (GPER1) on ?-Amyloid-Induced Neurotoxicity: Implications for Alzheimer's Disease

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dc.authoridUremis, Muhammed/0000-0003-2296-2422
dc.authoridBOSNAK, MEHMET/0000-0003-3491-5965
dc.authoridUremis, Muhammed Mehdi/0000-0003-2296-2422
dc.authorwosidAltun, I/A-6095-2016
dc.authorwosidUremis, Muhammed/V-5830-2019
dc.authorwosidKılıçaslan, Derya/JVZ-8872-2024
dc.authorwosidBOSNAK, MEHMET/ABI-5098-2020
dc.authorwosidUremis, Muhammed Mehdi/HKP-0531-2023
dc.contributor.authorKurt, Akif Hakan
dc.contributor.authorYuksel, Kasim Zafer
dc.contributor.authorUremis, Nuray
dc.contributor.authorUremis, Muhammed Mehdi
dc.contributor.authorAltun, Idiris
dc.contributor.authorBosnak, Mehmet
dc.contributor.authorKilicaslan, Derya
dc.date.accessioned2024-08-04T21:00:56Z
dc.date.available2024-08-04T21:00:56Z
dc.date.issued2019
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAlzheimer's disease (AD) is a problematic disease that has shown a significant increase in patient numbers worldwide. AD is identified pathologically by the accumulation of the toxic amyloid beta (A) protein, neurofibrillary tangles and neuropil threads in postmortem brains of AD patients. Women are more prone to AD either due to their increased life expectancy or the decline in Estrogen hormone levels around menopause. Estrogens play a physiologically important role in the brain, but there is debate about the association between estrogen and Ad. The neuroprotective effects of estrogens are possibly mediated by estrogen receptors (ERs), which include classical nuclear estrogen receptors (ER and ER) and nonclassical ER (G protein-coupled estrogen receptor 1, GPER1(GPR30)). The effect of GPER1 on A-induced neurotoxicity is unclear. Here we studied the effect of GPER1 receptor agonists G-1 on rat neuronal cells. Rat neuronal cells were incubated with A(1-42), either alone or in combination with GPER1 agonist G-1 (10(-7), 10(-8) and 10(-9) M). Cell viability was determined by MTT assays and apoptotic effects induced by A(1-42) were measured by Cell Death Detection kit. Oxidative stress parameters, including nitric oxide (NO) levels and total oxidant status (TOS) were measured by spectrophotometry. Approximately half of the cell death was observed with 10(-6) M A(1-42) incubation for 48 hours. This is the first study that explores the effect of activation of GPER1 by its agonist G-1 on neuroprotection against A(1-42)-toxicity in rat neuronal cells. GPER1 activation significantly reduced on rat neuronal cells. A(1-42) induced cell death was significantly reduced by co-incubating with G-1. Our results suggest that G-1 treatment protects neurons from A(1-42) induced neurotoxicity by changing the oxidative parameters on rat neuronal cells.en_US
dc.description.sponsorshipKahramanmaras Sutcu Imam University Research Foundationen_US
dc.description.sponsorshipThis study was supported by Kahramanmaras Sutcu Imam University Research Foundation.en_US
dc.identifier.doi10.1134/S1819712419010148
dc.identifier.endpage104en_US
dc.identifier.issn1819-7124
dc.identifier.issn1819-7132
dc.identifier.issue1en_US
dc.identifier.startpage99en_US
dc.identifier.urihttps://doi.org/10.1134/S1819712419010148
dc.identifier.urihttps://hdl.handle.net/11616/103944
dc.identifier.volume13en_US
dc.identifier.wosWOS:000466383700014en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.language.isoenen_US
dc.publisherMaik Nauka/Interperiodica/Springeren_US
dc.relation.ispartofNeurochemical Journalen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectGPER1en_US
dc.subjectneuronen_US
dc.subjectA beta(1-42)en_US
dc.subjectneurodegenerationen_US
dc.subjectNOen_US
dc.subjectapoptosisen_US
dc.titleProtective Effects of G Protein-Coupled Estrogen Receptor 1 (GPER1) on ?-Amyloid-Induced Neurotoxicity: Implications for Alzheimer's Diseaseen_US
dc.typeArticleen_US

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