The ameliorative effect of carvacrol on sodium arsenite-induced hepatotoxicity in rats: Possible role of Nrf2/HO-1, RAGE/NLRP3, Bax/Bcl-2/Caspase-3, and Beclin-1 pathways.

Autor: Gencer S; Department of Internal Diseases, Faculty of Medicine, Aksaray University, Aksaray, Turkey., Gür C; Department of Medical Laboratory Techniques, Vocational School of Health Services, Atatürk University, Erzurum, Turkey., İleritürk M; Department of Animal Science, Horasan Vocational College, Atatürk University, Erzurum, Turkey., Küçükler S; Department of Veterinary Biochemistry, Faculty of Veterinary, Atatürk University, Erzurum, Turkey., Akaras N; Department of Histology and Embryology, Faculty of Medicine, Aksaray University, Aksaray, Turkey., Şimşek H; Department of Physiology, Faculty of Medicine, Aksaray University, Aksaray, Turkey., Kandemir FM; Department of Medical Biochemistry, Faculty of Medicine, Aksaray University, Aksaray, Turkey.
Jazyk: angličtina
Zdroj: Journal of biochemical and molecular toxicology [J Biochem Mol Toxicol] 2024 Oct; Vol. 38 (10), pp. e23863.
DOI: 10.1002/jbt.23863
Abstrakt: Arsenic is a toxic environmental pollutant heavy metal, and one of its critical target tissues in the body is the liver. Carvacrol is a natural phytocompound that stands out with its antioxidant, anti-inflammatory, and antiapoptotic properties. The current study aims to investigate the protective feature of carvacrol against sodium arsenite-induced liver toxicity. Thirty-five Sprague-Dawley male rats were divided into five groups: Control, Sodium arsenite (SA), CRV, SA + CRV25, and SA + CRV50. Sodium arsenite was administered via oral gavage at a dose of 10 mg/kg for 14 days, and 30 min later, CRV 25 or 50 mg/kg was administered via oral gavage. Oxidative stress, inflammation, apoptosis, autophagy damage pathways parameters, and liver tissue integrity were analyzed using biochemical, molecular, western blot, histological, and immunohistological methods. Carvacrol decreased sodium arsenite-induced oxidative stress by suppressing malondialdehyde levels and increasing superoxide dismutase, catalase, glutathione peroxidase activities, and glutathione levels. Carvacrol reduced inflammation damage by reducing sodium arsenite-induced increased levels of NF-κB and the cytokines (TNF-α, IL-1β, IL-6, RAGE, and NLRP3) it stimulates. Carvacrol also reduced sodium arsenite-induced autophagic (Beclin-1, LC3A, and LC3B) and apoptotic (P53, Apaf-1, Casp-3, Casp-6, Casp-9, and Bax) parameters. Carvacrol preserved sodium arsenite-induced impaired liver tissue structure. Carvacrol alleviated toxic damage by reducing sodium arsenite-induced increases in oxidative stress, inflammation, apoptosis, and autophagic damage parameters in rat liver tissues. Carvacrol was also beneficial in preserving liver tissue integrity.
(© 2024 The Author(s). Journal of Biochemical and Molecular Toxicology published by Wiley Periodicals LLC.)
Databáze: MEDLINE
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