ACA, an inhibitor phospholipases A2 and transient receptor potential melastatin-2 channels, attenuates okadaic acid induced neurodegeneration in rats

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dc.authoridYologlu, Saim/0000-0002-9619-3462
dc.authoridCigremis, Yilmaz/0000-0002-8600-0946
dc.authoridCakir, Murat/0000-0002-2066-829X
dc.authoridTaslidere, Elif/0000-0003-1723-2556
dc.authoridTekin, Suat/0000-0002-2757-1802;
dc.authorwosidYologlu, Saim/ABI-8014-2020
dc.authorwosidCigremis, Yilmaz/JAC-8451-2023
dc.authorwosidCigremis, Yilmaz/O-6019-2015
dc.authorwosidCakir, Murat/I-8643-2019
dc.authorwosidTekin, Suat/AAG-1440-2021
dc.authorwosidTaslidere, Elif/ABI-8046-2020
dc.authorwosidÖzgöçer, Tuba/AAA-1751-2021
dc.contributor.authorCakir, Murat
dc.contributor.authorDuzova, Halil
dc.contributor.authorTekin, Suat
dc.contributor.authorTaslidere, Elif
dc.contributor.authorKaya, Gul Busra
dc.contributor.authorCigremis, Yilmaz
dc.contributor.authorOzgocer, Tuba
dc.date.accessioned2024-08-04T20:43:03Z
dc.date.available2024-08-04T20:43:03Z
dc.date.issued2017
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAim: In recent studies, it has been shown that the Transient Receptor Potential Melastatin-2 Channels (TRPM2) and Phospholipases A2 (PLA(2)) inhibitors may have a protective effect on neurons. This study was aimed to investigate the protective effect of TRPM2 and PLA(2) inhibitor N-(p-amylcinnamoyl) Anthranilic Acid (ACA) in a neurodegenerative model induced by Okadaic Acid (OKA). Main methods: OKA (200 ng/10 mu l) was administered bilateral intracerebroventricularly as a single injection. Key findings: OKA-treated rats showed significant impairments of spatial memory in Morris Water Maze Test. OKA-induced memory-impaired rats showed increased numbers of degenerated neurons and Caspase-3, tau phosphorylated ser396, beta-amyloid positive cells in the hippocampus and cerebral cortex. Furthermore, OKA-treated rats exhibited significantly increased MDA, TNF-alpha levels, and decreased SOD, GSH-PX enzyme activates and GSH levels of the tissues. ACA administration ameliorated OKA-induced memory impairment in rats. The ACA treatment also increased SOD and GSH-PX enzyme activation and GSH levels, and conversely decreased the levels of MDA, TNF-alpha. It was found that the numbers of the degenerated neurons and Caspase-3 positive cells of cortex and hippocampus regions were significantly reduced. Significance: ACA administration attenuates the oxidative stress and neuroinflammation of OKA-induced neurodegeneration; and ameliorates the cognitive decline and neurodegeneration. (C) 2017 Elsevier Inc. All rights reserved.en_US
dc.description.sponsorshipDepartment of Scientific Research Projects of Inonu University [2015/105]en_US
dc.description.sponsorshipThis study was supported by the Department of Scientific Research Projects of Inonu University (Project no: 2015/105). Competing interests declared.en_US
dc.identifier.doi10.1016/j.lfs.2017.03.022
dc.identifier.endpage20en_US
dc.identifier.issn0024-3205
dc.identifier.issn1879-0631
dc.identifier.pmid28363841en_US
dc.identifier.scopus2-s2.0-85016397485en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage10en_US
dc.identifier.urihttps://doi.org/10.1016/j.lfs.2017.03.022
dc.identifier.urihttps://hdl.handle.net/11616/97762
dc.identifier.volume176en_US
dc.identifier.wosWOS:000400537500002en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherPergamon-Elsevier Science Ltden_US
dc.relation.ispartofLife Sciencesen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectOkadaic aciden_US
dc.subjectN-(p-amylcinnamoyl) anthranilic acid (ACA)en_US
dc.subjectNeurodegenerationen_US
dc.subjectTRPM2 channelen_US
dc.subjectPhospholipases A(2)en_US
dc.subjectAlzheimer's diseaseen_US
dc.titleACA, an inhibitor phospholipases A2 and transient receptor potential melastatin-2 channels, attenuates okadaic acid induced neurodegeneration in ratsen_US
dc.typeArticleen_US

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