Zingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-?B, caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway

dc.contributor.authorYılmaz, Selçuk
dc.contributor.authorGür, Cihan
dc.contributor.authorKücükler, Sefa
dc.contributor.authorAkaras, Nurhan
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2024-07-08T11:01:13Z
dc.date.available2024-07-08T11:01:13Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractIn the present study, the potential protective effects of zingerone (ZNG) against sciatic nerve damage caused by sodium arsenite (SA), a common environmental pollutant, were evaluated by various biochemical, molecular, and histological methods. Materials and Methods: In the study, SA and ZNG were given to 35 male Sprague Dawley rats for 14 days. At the end of the period, the sciatic nerve tissues were taken and the markers involved in oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis were analyzed. Results: The data obtained showed that SA decreased glutathione (GSH) levels and increased malondialdehyde (MDA) levels in the sciatic nerve tissue. However, it was determined that these markers approached the control group levels due to the anti-oxidant properties of ZNG. While SA triggered endoplasmic reticulum stress and apoptosis pathways, ZNG suppressed them. Moreover, SA up-regulated inflammatory markers such as nuclear factor kappa-B (NF-?B), tumor necrosis factor-alpha (TNF-?), interleukin-1-beta (IL-1?), and neuronal nitric oxide synthases (nNOS) in the sciatic nerves and caused neuro-inflammation and inhibited cell survival by suppressing serine/threonineprotein kinase 2 (Akt2) and forkhead box protein O1 (FOXO1) genes. It has also been shown histopathologically that SA causes degeneration in the sciatic nerves. In contrast, ZNG suppressed neuro-inflammation, activated Akt2/FOXO1 signaling, and repaired histological irregularities. Conclusion: In general, SA caused oxidative stress, inflammation, ER stress, and apoptosis in the sciatic nerves of rats, causing damage to the tissues, however,
dc.identifier.doi10.22038/IJBMS.2023.74088.16094
dc.identifier.endpage491en_US
dc.identifier.issn2008-3866
dc.identifier.issue4en_US
dc.identifier.scopusqualityQ2
dc.identifier.startpage485en_US
dc.identifier.urihttps:/dx.doi.org/10.22038/IJBMS.2023.74088.16094
dc.identifier.urihttps://hdl.handle.net/20.500.12451/12086
dc.identifier.volume27en_US
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherMashhad University of Medical Sciences
dc.relation.ispartofIranian Journal of Basic Medical Sciences
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectApoptosis
dc.subjectEndoplasmic Reticulum-stress
dc.subjectInflammation
dc.subjectSciatic Nerve
dc.subjectSodium Arsenite
dc.titleZingerone attenuates sciatic nerve damage caused by sodium arsenite by inhibiting NF-?B, caspase-3, and ATF-6/CHOP pathways and activating the Akt2/FOXO1 pathway
dc.typeArticle

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