Naringin alleviates liver damage induced by D-galactosamine (D-gal) in mice through down-regulation of CYP2E1 and P53 hyperactivity

This study aims to study the potential antioxidants and the anti-inflammatory effects of naringin in mice-induced liver damage by D-galactosamine (D-gal) administration. Mice were divided into four groups: group 1, the normal control group; group 2, the D-gal group was injected (200  mg /kg; s.c.) daily for 8 weeks; and groups 3 and 4, naringin groups received naringin (150 mg/kg and 300 mg/kg; p.o.) daily concurrent with D-gal for 8 weeks. Serum was prepared to measure aspartate transaminase (AST) and alanine transaminases (ALT). Liver tissue homogenate was prepared to me asure nitric oxide (NO), catalase, cytochrome P450 2E1(CYP2E1), tumor necrotic factor (TNF- α), C-X-C motif chemokine ligand 1 (CXCL1), and CD44. Finally, histological and immunohistochemical studies were performed. Supplementation with naringin for 8 weeks significantly decreased the levels of AST, ALT, CYP2E1, TNF-α, CXCL1, and CD44, and pathology of the liver showed improvement of tr eated groups with increased dose as hepatic cells showed signs of regeneration with binucleated hepatic cells with normal hepatic architecture and suppressed P53 hyperactivity as an apoptotic marker. Naringin exhibited hepatoprotective effects in mice by inhibiting reactive oxygen species (ROS), dow n-regulating of CYP2E1 liver content, and producing a significant decline in different inflammatory markers as well as suppressing apoptosis.
Source: Comparative Clinical Pathology - Category: Pathology Source Type: research