Therapeutic effects of carvacrol on beta-amyloid-induced impairments in in vitro and in vivo models of Alzheimer's disease

dc.authoridKılınç, Erkan/0000-0001-9261-2634
dc.authorwosidKılınç, Erkan/A-4015-2017
dc.contributor.authorTopkara, Kübra Çelik
dc.contributor.authorKılınç, Erkan
dc.contributor.authorÇetinkaya, Ayhan
dc.contributor.authorSaylan, Asıihan
dc.contributor.authorDemir, Şerif
dc.date.accessioned2023-07-26T11:53:51Z
dc.date.available2023-07-26T11:53:51Z
dc.date.issued2022
dc.departmentDÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Fizyoloji Ana Bilim Dalıen_US
dc.description.abstractDue to the complex nature of Alzheimer's disease (AD), it is important to investigate agents with multiple effects in the treatment of AD. Carvacrol possesses anti-acetylcholinesterase, anti-oxidant, and neuroprotective properties. We therefore investigated therapeutic effects of carvacrol on cell viability, oxidative stress, and cognitive impairment in A beta 1-42-induced in vitro and in vivo models of AD. SH-SY5Y cells differentiated into neurons by retinoic acid were pretreated with carvacrol or galantamine before A beta 1-42 administration. For in vivo experiments, a rat model of AD was established by bilateral intrahippocampal injection of A beta 1-42. The groups received 1% DMSO, carvacrol, or galantamine intraperitoneally twice a day (morning and afternoon) for 6 days. Cell viability was determined using MTT and LDH tests. Learning and memory functions were assessed using a passive-avoidance test. Oxidant-antioxidant parameters (MDA, H2O2, SOD, and CAT) and Tau, A beta 1-40, and A beta 1-42 peptide levels in in vitro supernatant or in vivo serum and hippocampal samples were measured using ELISA. Carvacrol increased cell viability and exhibited a protective effect against oxidative stress by preventing A beta 1-42-induced cytotoxicity, LDH release, and increments in MDA and H2O2 levels in vitro. Additionally, it improved memory impairment by reversing A beta 1-42-induced changes on passive-avoidance test. Carvacrol ameliorated A beta 1-42-induced increments in MDA and H2O2 levels in in vitro supernatant and in vivo hippocampal samples. However, none of the treatments changed in vitro SOD and Tau-peptide levels, or in vivo serum levels of MDA, H2O2, SOD, CAT, Tau peptide, A beta 1-40, or A beta 1-42. Our results suggest that multi-target pharmacological agent carvacrol may be promising in treatment of AD by preventing beta-amyloid-induced neurotoxicity, oxidative stress, and memory deficits.en_US
dc.description.sponsorshipBolu Abant Izzet Baysal University Scientific Research Fund [2018.08.02.1364]en_US
dc.description.sponsorshipThis study was supported by the Bolu Abant Izzet Baysal University Scientific Research Fund (grant number 2018.08.02.1364).en_US
dc.identifier.doi10.1111/ejn.15565
dc.identifier.endpage5726en_US
dc.identifier.issn0953-816X
dc.identifier.issn1460-9568
dc.identifier.issue9en_US
dc.identifier.pmid34904309en_US
dc.identifier.scopus2-s2.0-85121508881en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage5714en_US
dc.identifier.urihttps://doi.org/10.1111/ejn.15565
dc.identifier.urihttps://hdl.handle.net/20.500.12684/12631
dc.identifier.volume56en_US
dc.identifier.wosWOS:000733339000001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorDemir, Şerif
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofEuropean Journal of Neuroscienceen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz$2023V1Guncelleme$en_US
dc.subjectAlzheimer's Disease; Carvacrol; Memory; Neurotoxicity; Oxidative Stress; Sh-Sy5y Cellsen_US
dc.subjectMild Cognitive Impairment; Transgenic Mouse Model; Oxidative Stress; Cholinergic Neurons; Lipid-Peroxidation; Protein; Neuroinflammation; Peptide; Thymol; Memoryen_US
dc.titleTherapeutic effects of carvacrol on beta-amyloid-induced impairments in in vitro and in vivo models of Alzheimer's diseaseen_US
dc.typeArticleen_US

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