4.0 Article

Role of Quercetin in Preventing Thioacetamide-Induced Liver Injury in Rats

Journal

TOXICOLOGIC PATHOLOGY
Volume 39, Issue 6, Pages 949-957

Publisher

SAGE PUBLICATIONS INC
DOI: 10.1177/0192623311418680

Keywords

quercetin; thioacetamide; hepatotoxicity; oxidative stress

Funding

  1. FIPE: Fundo de Incentivo a Pesquisa e Eventos
  2. CNPq: Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (National Council for Scientific and Technological Development)
  3. CAPES (Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior)

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In hepatic toxicity induced in rats by two injections of thioacetamide (TAA, 350 mg/kg with an interval of 8 hr), the action of quercetin was investigated. After 96 hr, TAA administration resulted in hepatic necrosis, significant increases in serum transaminase activity, and increases in hepatic lipoperoxidation. Thioacetamide-induced hepatotoxicity also showed changes in antioxidant enzymes in the liver of rats, with alterations in p-ERK1/2 (phosphorylated extracellular-signal related kinase 1/2) as well as an imbalance between proapototic protein Bax and anti-apoptotic protein Bcl-2 expression. With administration of the flavonoid quercetin (50 mg/Kg i.p.) for four consecutive days following TAA, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity were close to normal values in rats. Histological findings suggested that quercetin had a preventive effect on TAA-induced hepatic necrosis. Quercetin treatment caused significant decreases in lipid peroxide levels in the TAA-treated rats, with some changes in antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Quercetin also inhibited the change of the p-ERK1/2 by TAA and significantly prevented the increase in Bax/Bcl-2 ratio, thus preventing apoptosis. Findings indicate that quercetin may have a preventive effect on TAA-induced hepatotoxicity by modulating the oxidative stress parameters and apoptosis pathway.

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