Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B1-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway

Aflatoxin B1(AFB1) exists widely in feed and food with severe hazards, posing a serious threat to human and animal health. Epigallocatechin gallate (EGCG) and glutathione (GSH) have been reported as having anti-oxidative and other functions. The present study aimed to investigate the detoxification effect of EGCG and GSH alone or in combination on AFB1exposure in ducklings. Fifty one-day-old male ducklings were randomly assigned into five experimental groups (n= 10): 1. Control (CTR); 2. 0.3 mg/kg BW AFB1(AFB1); 3. 0.3 mg/kg BW AFB1+ 100 mg/kg BW EGCG (AFB1+ EGCG); 4. 0.3 mg/kg BW AFB1+ 30 mg/kg BW GSH (AFB1+ GSH); 5. 0.3 mg/kg BW AFB1+ 100 mg/kg BW EGCG + 30 mg/kg BW GSH (AFB1+ EGCG + GSH). The experiment lasted for seven days. Compared with the CTR group, AFB1reduced growth performance, total serum protein and albumin content, increased serum enzyme activity (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transpeptidase), and caused pathological damage to the ducklings’ livers. AFB1exposure increased malondialdehyde content and decreased superoxide dismutase, total antioxidant capacity, catalase, glutathione peroxidase activities, and glutathione content in the liver. EGCG and GSH alone or in combination mitigated these adverse effects. Meanwhile, EGCG and GSH attenuate apoptosis of hepatocytes, and regulated AFB1-induced changes in the abundance of genes contained in the Keap1/Nrf2 signalling and apoptotic pathways. Collectively, these results suggest that EGCG and GSH alleviate the hepatocyte injury induced by AFB1by inhibiting oxidative stress and attenuating excessive mitochondria-mediated apoptosis.Keywords:aflatoxin B1;duckling;epigallocatechin gallate;glutathione;oxidative stress;Keap1/Nrf2 signalling;apoptosisKey Contribution:EGCG and GSH alleviate AFB1-induced liver injury in ducklings by increasing antioxidant capacity and antagonising apoptosis.