Protective effects of zingerone against sodium arsenite-induced lung toxicity: A multi-biomarker approach
dc.contributor.author | Şimşek, Hasan | |
dc.contributor.author | Küçükler, Sefa | |
dc.contributor.author | Gür, Cihan | |
dc.contributor.author | İleritürk, Mustafa | |
dc.contributor.author | Aygörmez, Serpil | |
dc.contributor.author | Kandemir, Fatih Mehmet | |
dc.date.accessioned | 2023-09-28T06:31:36Z | |
dc.date.available | 2023-09-28T06:31:36Z | |
dc.date.issued | 2023 | |
dc.department | Tıp Fakültesi | |
dc.description.abstract | Sodium arsenite (SA) exposure is toxic to the body. Zingerone (ZNG) is a flavonoid with many biological properties found naturally in honey and plants. This study aimed to determine the effects of ZNG on SA-induced rat lung toxicity. Materials and Methods: Thirty-five male Sprague rats were divided into Control, SA, ZNG, SA+ZNG25, and SA+ZNG50 groups (n=7). SA 10 mg/kg and ZNG were administered at two doses (25 and 50 mg/kg) (orally, 14 days). Analysis of oxidative stress, inflammation damage, apoptosis damage, and autophagic damage markers in lung tissue were determined by biochemical and histological methods. Results: The administration of ZNG reduced oxidative stress by increasing SA-induced decreased antioxidant enzyme activities, increasing Nrf-2, HO-1, and NQO1, and decreasing MDA level. ZNG administration reduced inflammation marker levels. Anti-apoptotic Bcl-2 increased and apoptotic Bax and Caspase-3 decreased with ZNG. ZNG promoted the regression of autophagy by reducing Beclin-1, LC3A, and LC3B levels. Conclusion: Evaluating all data showed that SA caused toxic damage to lung tissue by increasing inflammation, apoptosis, autophagy, and oxidant levels, whereas ZNG had a protective effect by reducing this damage. | |
dc.identifier.doi | 10.22038/IJBMS.2023.71905.15623 | |
dc.identifier.endpage | 1106 | en_US |
dc.identifier.issn | 2008-3866 | |
dc.identifier.issue | 9 | en_US |
dc.identifier.pmid | 37605724 | |
dc.identifier.scopusquality | Q2 | |
dc.identifier.startpage | 1098 | en_US |
dc.identifier.uri | https:/dx.doi.org10.22038/IJBMS.2023.71905.15623 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12451/10994 | |
dc.identifier.volume | 26 | en_US |
dc.identifier.wos | WOS:001041104000015 | |
dc.identifier.wosquality | Q3 | |
dc.indekslendigikaynak | Web of Science | |
dc.indekslendigikaynak | Scopus | |
dc.indekslendigikaynak | PubMed | |
dc.language.iso | en | |
dc.publisher | Mashhad University of Medical Sciences | |
dc.relation.ispartof | Iranian Journal of Basic Medical Sciences | |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | |
dc.rights | info:eu-repo/semantics/closedAccess | |
dc.subject | Apoptosis | |
dc.subject | Autophagy | |
dc.subject | Inflammation | |
dc.subject | Lung | |
dc.subject | Oxidative Stress | |
dc.subject | Sodium Arsenite | |
dc.subject | Toxicity | |
dc.subject | Zingerone | |
dc.title | Protective effects of zingerone against sodium arsenite-induced lung toxicity: A multi-biomarker approach | |
dc.type | Article |