Protective effects of silymarin on fumonisin B-1-induced hepatotoxicity in mice


Sozmen M., Devrim A. K., TUNCA R., Bayezit M., DAĞ S., Essiz D.

JOURNAL OF VETERINARY SCIENCE, cilt.15, sa.1, ss.51-60, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 15 Sayı: 1
  • Basım Tarihi: 2014
  • Doi Numarası: 10.4142/jvs.2014.15.1.51
  • Dergi Adı: JOURNAL OF VETERINARY SCIENCE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.51-60
  • Anahtar Kelimeler: caspase-8, fumonisin B1, fibroblast growth factor-2, galectin-3, silymarin, ENDOTHELIAL GROWTH-FACTOR, SIGNALING GENES, MOUSE-LIVER, EXPRESSION, B-1, GALECTIN-3, APOPTOSIS, ANGIOGENESIS, REGENERATION, INHIBITION
  • Ondokuz Mayıs Üniversitesi Adresli: Hayır

Özet

The present study was conducted to investigate the effect of silymarin on experimental liver toxication induced by Fumonisin B-1 (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.