Protective effects of zingerone against sodium arsenite-induced lung toxicity: A multi-biomarker approach

被引:15
作者
Simsek, Hasan [1 ]
Kucukler, Sefa [2 ]
Gur, Cihan [2 ]
Ileriturk, Mustafa [3 ]
Aygormez, Serpil [4 ]
Kandemir, Fatih Mehmet [5 ]
机构
[1] Aksaray Univ, Fac Med, Dept Physiol, Aksaray, Turkiye
[2] Ataturk Univ, Fac Vet, Dept Vet Biochem, Erzurum, Turkiye
[3] Ataturk Univ, Horasan Vocat Coll, Dept Anim Sci, Erzurum, Turkiye
[4] Kafkas Univ, Fac Vet, Dept Vet Biochem, Kars, Turkiye
[5] Aksaray Univ, Fac Med, Dept Med Biochem, Aksaray, Turkiye
关键词
Apoptosis; Autophagy; Inflammation; Lung; Oxidative stress; Sodium arsenite; Toxicity; Zingerone; OXIDATIVE STRESS; INFLAMMATION; INJURY; APOPTOSIS;
D O I
10.22038/IJBMS.2023.71905.15623
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Objective(s): 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 andMethods: 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.
引用
收藏
页码:1098 / 1106
页数:9
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