Akademik Veri Yönetim Sistemi
Revista Cientifica de la Facultad de Veterinaria, cilt.35, sa.1, ss.1-8, 2025 (SCI-Expanded)
Aflatoxicosis, a mycotoxicosis caused by aflatoxins, poses significant economic challenges in animal husbandry and presents serious health risks to humans. The current study aimed to evaluate the protective effects of Silymarin, an antioxidant, against aflatoxicosis in broiler chickens. A total of thirty–two broilers were randomly assigned to four experimental groups: control, Silymarin– treated, Aflatoxin B1 (AFB1)–treated, and AFB1+Silymarin–treated. Broilers in control and Silymarin–treated groups were fed with a diet without Aflatoxin. AFB1 and AFB1+Silymarin treated groups received approximately 1 mg of Aflatoxin/broiler/total for 21 days. AFB1+Silymarin group also received 10 g of Silymarin kg–1 of food as a supplementation diet for 21 days. Biochemically, liver and serum TAS, SOD, GSH–Px, CAT, and BcL–2 levels in the AFB1 group were lower than the control, while serum TOS, and serum and liver Caspase–3 levels were high (P<0.001). In addition, in the AFB1+Silymarin group, liver and serum GSH–Px, SOD and BcL–2, and serum CAT values were significantly higher than the AFB1 group (P<0.001). Also, in the AFB1+Silymarin group, there was a slight increase in CAT level in liver samples compared to the AFB1 group (P>0.05). Furthermore, TOS and Caspase–3 levels of both serum and liver in the AFB1+Silymarin group were low, while BcL–2 levels were quite high in serum samples compared to the AFB1 group (P<0.001). Pathologically, the livers were larger and pale in the AFB1 group. Histopathological analysis of the AFB1– treated group revealed diffuse hydropic/vacuolar degeneration and fibrosis, characterized by the activation of perisinusoidal myofibroblastic (Ito) cells. These morphological changes were significantly reduced in the AFB1+Silymarin group. These findings indicate that Silymarin, with its strong antioxidant effect, may be effective against aflatoxicosis in preventing liver damage in broilers.