The present study was conducted to investigate the effect of silymarin on experimental liver toxication induced by Fumonisin B₁1 (FB₁) in BALB/c mice. The mice were divided into six groups (n = 15). Group 1 served as the control. Group 2 was the silymarin control (100 mg/kg by gavage). Groups 3 and 4 were treated with FB₁ (Group 3, 1.5 mg/kg FB₁, intraperitoneally; and Group 4, 4.5 mg/kg FB₁). Group 5 received FB₁ (1.5 mg/kg) and silymarin (100 mg/kg), and Group 6 was given a higher dose of FB₁ (4.5 mg/kg FB₁) with silymarin (100 mg/kg). Silymarin treatment significantly decreased (p < 0.0001) the apoptotic rate. FB1 administration significantly increased (p < 0.0001) proliferating cell nuclear antigen and Ki-67 expression. Furthermore, FB1 elevated the levels of caspase-8 and tumor necrosis factor-alpha mediators while silymarin significantly reduced (p < 0.0001) the expression of these factors. Vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) expressions were significantly elevated in Group 4 (p < 0.0001). Silymarin administration alleviated increased VEGF and FGF-2 expression levels (p < 0.0001). In conclusion, silymarin ameliorated toxic liver damage caused by FB₁ in BALB/c mice.
Keywords: caspase-8; fibroblast growth factor-2; fumonisin B1; galectin-3; silymarin.