Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B1-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway
2022
Yanan Wang | Jiayu Wu | Lingfeng Wang | Ping Yang | Zuhong Liu | Shahid Ali Rajput | Mubashar Hassan | Desheng Qi
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 AFB1 exposure 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, AFB1 reduced growth performance, total serum protein and albumin content, increased serum enzyme activity (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and &gamma:-glutamyl transpeptidase), and caused pathological damage to the ducklings&rsquo: livers. AFB1 exposure 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 AFB1 by inhibiting oxidative stress and attenuating excessive mitochondria-mediated apoptosis.
Mostrar más [+] Menos [-]Palabras clave de AGROVOC
Información bibliográfica
Este registro bibliográfico ha sido proporcionado por Multidisciplinary Digital Publishing Institute