Effect of Three PDEIs on Neuroprotective and Autophagy Proteins in vitro AD Model

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dc.contributor.authorSaygisever-Faikoglu, Kubra
dc.contributor.authorFaikoglu, Gokhan
dc.contributor.authorCelik, Hande
dc.contributor.authorUgur, Sedat Askin
dc.contributor.authorAkkan, Ahmet Gokhan
dc.contributor.authorKelicen-Ugur, Pelin
dc.contributor.authorOzyazgan, Sibel
dc.date.accessioned2024-03-13T10:33:17Z
dc.date.available2024-03-13T10:33:17Z
dc.date.issued2021
dc.departmentİstanbul Beykent Üniversitesien_US
dc.description.abstractBackground and Objective: The effects of PDEIs on neuroprotective SIRT1 and SESN2, on the autophagy-related proteins, are unknown but neuroprotective enzymes (sirtuins and sestrins) with autophagy genes are involved in the pathogenesis of Alzheimer's disease. In this study, we aimed to elucidate the effect of three PDE Inhibitors (PDEIs) as autophagy enhancers and provide insights into their neuroprotective effects. Materials and Methods: HT-22 cells were exposed to A$ 25-35 with or without PDEIs for 32 hrs. qRT-PCR was performed for SIRT1, SESN2, ATG5 and BECN1 genes. Western blot analysis was performed for neuroprotective SIRT1, SESN2 proteins and autophagy proteins such as p-mTOR/mTOR, p-AMPK/AMPK and LC3. Results: A$ 25-35 exposure decreased SIRT1, ATG5 and BECN1 expression, while PDEIs prevented these genes from the A$ 25-35 induced decrease. Increased SESN2 gene expression by A$ 25-35 exposure was decreased by PDEIs treatment. Western blot experiment has also shown that SIRT1, p-AMPK and autophagy marker LC3II were decreased, whereas SESN2 and p-mTOR were elevated in the A$ 25-35 exposed HT-22 cells. Co administration of three PDEIs with A$ 25-35 recovered SIRT1, p-AMPK and LC3II decline and compensated SESN2 increase by elevating SIRT1, p-AMPK and LC3II expression and decreasing p-mTOR expression. Conclusion: The present study revealed the significant neuroprotective and autophagy stimulating potential of three PDEIs in A$-induced in vitro AD model. SIRT1 is a novel candidate for determining new, safe and effective treatment strategies and PDEI-mediated SIRT1 increase may advocate autophagy activation through different autophagy components.en_US
dc.identifier.doi10.3923/ijp.2021.169.179
dc.identifier.endpage179en_US
dc.identifier.issn1811-7775
dc.identifier.issn1812-5700
dc.identifier.issue4en_US
dc.identifier.startpage169en_US
dc.identifier.urihttps://doi.org/10.3923/ijp.2021.169.179
dc.identifier.urihttps://hdl.handle.net/20.500.12662/3868
dc.identifier.volume17en_US
dc.identifier.wosWOS:000704553400002
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Science
dc.language.isoenen_US
dc.publisherAsian Network Scientific Information-Ansineten_US
dc.relation.ispartofInternational Journal Of Pharmacologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectPDEIsen_US
dc.subjectSirtuin-1en_US
dc.subjectSestrin-2en_US
dc.subjectAMPK/mTORen_US
dc.subjectAlzheimer's diseaseen_US
dc.subjectautophagyen_US
dc.subjectWestern bloten_US
dc.titleEffect of Three PDEIs on Neuroprotective and Autophagy Proteins in vitro AD Modelen_US
dc.typeArticleen_US

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