Hepatoprotective effects of epigallocatechin gallate and glutathione on aflatoxin B1-induced subacute liver injury in ducklings.

Aflatoxin B1 (AFB1) is found extensively in grains and complete feed. In poultry, AFB1-contaminated feed will cause severe liver damage, especially in ducklings. This research aimed to investigate the effects and mechanisms of epigallocatechin gallate (EGCG) and glutathione (GSH) on AFB1-induced subacute liver injury in ducklings. Ducklings were fed a diet containing 80 μg/kg of AFB1 and administered EGCG (400 mg/kg) and GSH (120 mg/kg) either alone or in combination for four weeks. AFB1 caused more serious effects at week 2 compared to week 4 based on the analyses of growth performance, liver index, and hepatic function parameters. Therefore, all other indicators were examined using samples collected at week 2. The results showed that EGCG and GSH mitigated the negative effects of AFB1 on growth, hepatic microstructure and ultrastructure, and liver function of ducklings. Meanwhile, EGCG and GSH downregulated the expression of cytochrome P450 (CYP450) enzyme system genes, inhibited the production of malondialdehyde (MDA), upregulated the expression of nuclear factor E2-related factor 2 (Nrf2), NADPH quinone oxidoreductase 1 (NQO1), superoxide dismutase 1 (SOD1), and glutathione S-transferase (GST), and increased the activity of SOD and glutathione peroxidase (GPX). AFB1-induced hepatocyte apoptosis was also counteracted by EGCG and GSH through the regulation of mitochondrial apoptosis pathway genes. Furthermore, EGCG and GSH reduced the liver fibrosis rate by regulating the TGF-β/Smads signaling pathway and improved bile acid metabolism disruption. These results indicate that EGCG and GSH alleviate AFB1-induced liver damage in ducklings by regulating AFB1 metabolism, enhancing hepatic antioxidant capacity, reducing hepatocyte apoptosis and the level of liver fibrosis, and mediating the metabolism of bile acids.