The present study was conducted to investigate the effect of silymarin on experimental liver toxication induced by Fumonisin B1 (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.
Animals ; Antioxidants/*pharmacology ; Apoptosis/drug effects ; Cell Proliferation/drug effects ; Female ; Fibroblast Growth Factor 2/genetics/metabolism ; Fumonisins/*toxicity ; Gene Expression Regulation/drug effects ; Hepatocytes/*drug effects ; Ki-67 Antigen/metabolism ; Liver/drug effects ; Mice ; Mice, Inbred BALB C ; Mycotoxins/*toxicity ; Neovascularization, Physiologic/drug effects ; Proliferating Cell Nuclear Antigen/metabolism ; Silymarin/*pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; Vascular Endothelial Growth Factor A/genetics/metabolism