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

Document Type : Original Article

Authors

1 Department of Physiology, Faculty of Medicine, Aksaray University, Aksaray, Türkiye

2 Department of Veterinary Biochemistry, Faculty of Veterinary, Atatürk University, Erzurum, Türkiye

3 Department of Animal Science, Horasan Vocational College, Ataturk University, Erzurum, Türkiye

4 Department of Veterinary Biochemistry, Faculty of Veterinary, Kafkas University, Kars, Türkiye

5 Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Türkiye

Abstract

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 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.

Keywords

Main Subjects


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