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This work conducted to evaluate the anti-fibrotic and antioxidant role of naringenin (NAR) toward thioacetamide (TAA) induced liver fibrosis. Fifty adult male albino rats randomly divided into 5 groups (10 each); first group kept as control one; the second treated I/P by 200 mg/kg TAA twice a weeks for 8 weeks; the third was gavaged daily with 50 mg /kg/ b.wt of NAR; the fourth was co-treated by TAA and NAR while the fifth was treated with TAA for 8 w then gavaged daily by NAR for 1 month. TAA administration significantly increases the hepatic cell enzymes (ALT, AST, ALP and GGT) in the serum referring to hepatic cell destruction with an increase in hepatic MDA with a reduction in GSH concentrations, antioxidant enzyme activities as well as down regulation of their expression levels. NAR administration either with or after TAA ameliorates this effect suggesting its antioxidant ability. In the fibrotic pathway, TAA treatment up-regulates the expression levels of fibrogenic biomarkers (TGF-β, collagen 1α and fibronectin) genes while NAR down-regulates these genes suggesting its anti-fibrotic ability. Histopathological analysis confirms the biochemical results. In conclusion, NAR ameliorates the deleterious effect of TAA through its antioxidant and anti-fibrotic abilities.
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Ali et al. (2022) studied this question.
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