Şimşek, HasanKüçükler, SefaGür, Cihanİleritürk, MustafaAygörmez, SerpilKandemir, Fatih Mehmet2023-09-282023-09-2820232008-3866https:/dx.doi.org10.22038/IJBMS.2023.71905.15623https://hdl.handle.net/20.500.12451/10994Sodium 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.eninfo:eu-repo/semantics/closedAccessApoptosisAutophagyInflammationLungOxidative StressSodium ArseniteToxicityZingeroneArticle2691098110610.22038/IJBMS.2023.71905.1562337605724Q2WOS:001041104000015Q3