Neurochemical Research of LOXBlock-1 and ZnSO4 against Neurodegenerative Damage Induced by Amyloid Beta(1-42)

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dc.authoridSahin, Meryem Cansu/0000-0002-5743-3734en_US
dc.authoridKAR, FATIH/0000-0001-8356-9806en_US
dc.authoridHacioglu, Ceyhan/0000-0002-0993-6118en_US
dc.authorscopusid57208671422en_US
dc.authorscopusid57208669078en_US
dc.authorscopusid57210114831en_US
dc.authorwosidSahin, Meryem Cansu/HPG-1765-2023en_US
dc.contributor.authorHacioglu, Ceyhan
dc.contributor.authorKar, Fatih
dc.contributor.authorSahin, Meryem Cansu
dc.date.accessioned2024-08-23T16:07:04Z
dc.date.available2024-08-23T16:07:04Z
dc.date.issued2024en_US
dc.departmentDüzce Üniversitesien_US
dc.description.abstractSynaptosomes offer an intriguing ex vivo model system for investigating the molecular mechanisms of neurodegenerative processes. Lipoxygenases significantly affect the course of neurodegenerative diseases. Homeostasis of trace elements such as zinc is necessary for the continuity of brain functions. In this study, we purpose to determine whether LOXBlock-1, a 12/15 lipoxygenase inhibitor, and zinc sulfate (ZnSO4) provide any biochemical protection during neurodegenerative damage in synaptosomes induced by amyloid beta 1-42 (A beta 1-42). In this study, animals (30 Wistar Albino male rats 30) were divided into 5 groups (6 animals in each group): Control, 10 mu M A beta 1-42, 10 mu M A beta 1-42+25mM LOXBlock-1, 10 mu M A beta 1-42+10 mu M ZnSO4, and 10 mu M A beta 1-42+25mM LOXBlock-1+10 mu M ZnSO4. Synaptosomes were isolated from the rat cerebral cortex. Following, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, malondialdehyde (MDA) levels, adenosine deaminase (ADA) levels, reduced-glutathione (GSH) levels, neuronal nitric oxide synthase (nNOS) levels, acetylcholinesterase (AChE) activity, catalase (CAT) activity, and 8-OHdG levels in synaptosomes were detected according to the ELISA method. ADA and AChE expression and protein levels were analyzed. MDA, nNOS, AChE, and 8-OHdG levels in synaptosomes treated with A beta 1-42 resulted in an increase, while there was a decrease in ADA, GSH, and CAT levels (p<0.001 vs. control). Conversely, LOXBlock-1 and ZnSO4 treatments in synaptosomes treated with A beta 1-42 decreased MDA, nNOS, AChE, and 8-OHdG levels, while ADA, GSH, and CAT levels increased. Moreover, the most effective improvement was seen in the co-treatment group of LOXBlock-1 and ZnSO4. Our data showed that LOXBlock-1 and ZnSO4 co-treatment may protect against A beta 1-42 exposure in rat brain synaptosomes.en_US
dc.identifier.doi10.1007/s12011-023-03908-5
dc.identifier.endpage3214en_US
dc.identifier.issn0163-4984
dc.identifier.issn1559-0720
dc.identifier.issue7en_US
dc.identifier.pmid37872362en_US
dc.identifier.scopus2-s2.0-85174633901en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpage3204en_US
dc.identifier.urihttps://doi.org/10.1007/s12011-023-03908-5
dc.identifier.urihttps://hdl.handle.net/20.500.12684/14469
dc.identifier.volume202en_US
dc.identifier.wosWOS:001095803800003en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringernatureen_US
dc.relation.ispartofBiological Trace Element Researchen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAlzheimer's diseasesen_US
dc.subjectLOXBlock-1en_US
dc.subjectNitrosative stressen_US
dc.subjectOxidative stressen_US
dc.subjectSynaptosomeen_US
dc.subjectZinc sulfateen_US
dc.subjectAlzheimers-Diseaseen_US
dc.subjectOxidative Stressen_US
dc.subjectMemory Deficitsen_US
dc.subjectA-Betaen_US
dc.subjectBrainen_US
dc.subjectZincen_US
dc.subjectTauen_US
dc.subject12/15-Lipoxygenaseen_US
dc.subjectDysfunctionen_US
dc.subjectInhibitionen_US
dc.titleNeurochemical Research of LOXBlock-1 and ZnSO4 against Neurodegenerative Damage Induced by Amyloid Beta(1-42)en_US
dc.typeArticleen_US

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