Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways

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dc.contributor.authorTuncer, Sibel Çi?dem
dc.contributor.authorGür, Cihan
dc.contributor.authorKüçükler, Sefa
dc.contributor.authorAkarsu, Serkan Ali
dc.contributor.authorKandemir, Fatih Mehmet
dc.date.accessioned2024-07-04T05:44:33Z
dc.date.available2024-07-04T05:44:33Z
dc.date.issued2024
dc.departmentTıp Fakültesi
dc.description.abstractThis study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA). Materials and Methods: In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days. Results: As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-?B, TNF-?, IL-1?, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality. Conclusion: ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.
dc.identifier.doi10.22038/IJBMS.2024.73342.15934
dc.identifier.endpage610en_US
dc.identifier.issn2008-3866
dc.identifier.issue5en_US
dc.identifier.scopusqualityQ2
dc.identifier.startpage603en_US
dc.identifier.urihttps:/dx.doi.org/10.22038/IJBMS.2024.73342.15934
dc.identifier.urihttps://hdl.handle.net/20.500.12451/12042
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/embargoedAccess
dc.subjectApoptosis
dc.subjectInflammation
dc.subjectOxidative Stress
dc.subjectSodium Arsenite
dc.subjectTesticular Toxicity
dc.titleEffects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways
dc.typeArticle

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