Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway
Aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) 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...
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MDPI AG
2022-12-01
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| Series: | Toxins |
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| Online Access: | https://www.mdpi.com/2072-6651/14/12/876 |
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| author | Yanan Wang Jiayu Wu Lingfeng Wang Ping Yang Zuhong Liu Shahid Ali Rajput Mubashar Hassan Desheng Qi |
| author_facet | Yanan Wang Jiayu Wu Lingfeng Wang Ping Yang Zuhong Liu Shahid Ali Rajput Mubashar Hassan Desheng Qi |
| author_sort | Yanan Wang |
| collection | DOAJ |
| description | Aflatoxin B<sub>1</sub> (AFB<sub>1</sub>) 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 AFB<sub>1</sub> exposure in ducklings. Fifty one-day-old male ducklings were randomly assigned into five experimental groups (<i>n</i> = 10): 1. Control (CTR); 2. 0.3 mg/kg BW AFB<sub>1</sub> (AFB<sub>1</sub>); 3. 0.3 mg/kg BW AFB<sub>1</sub> + 100 mg/kg BW EGCG (AFB<sub>1</sub> + EGCG); 4. 0.3 mg/kg BW AFB<sub>1</sub> + 30 mg/kg BW GSH (AFB<sub>1</sub> + GSH); 5. 0.3 mg/kg BW AFB<sub>1</sub> + 100 mg/kg BW EGCG + 30 mg/kg BW GSH (AFB<sub>1</sub> + EGCG + GSH). The experiment lasted for seven days. Compared with the CTR group, AFB<sub>1</sub> reduced 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. AFB<sub>1</sub> 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 AFB<sub>1</sub>-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 AFB<sub>1</sub> by inhibiting oxidative stress and attenuating excessive mitochondria-mediated apoptosis. |
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| id | doaj.art-fda59312c75946d5935b74de9be0596e |
| institution | Directory Open Access Journal |
| issn | 2072-6651 |
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| spelling | doaj.art-fda59312c75946d5935b74de9be0596e2023-11-24T18:27:19ZengMDPI AGToxins2072-66512022-12-01141287610.3390/toxins14120876Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling PathwayYanan Wang0Jiayu Wu1Lingfeng Wang2Ping Yang3Zuhong Liu4Shahid Ali Rajput5Mubashar Hassan6Desheng Qi7Department of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaInstitute of Animal Husbandry and Veterinary Sciences, Wuhan Academy of Agricultural Sciences, Wuhan 430208, ChinaDepartment of Animal Feed and Production, Faculty of Veterinary and Animal Sciences, Muhammad Nawaz Shareef University of Agriculture, Multan 66000, PakistanDepartment of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaDepartment of Animal Nutrition and Feed Science, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, ChinaAflatoxin B<sub>1</sub> (AFB<sub>1</sub>) 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 AFB<sub>1</sub> exposure in ducklings. Fifty one-day-old male ducklings were randomly assigned into five experimental groups (<i>n</i> = 10): 1. Control (CTR); 2. 0.3 mg/kg BW AFB<sub>1</sub> (AFB<sub>1</sub>); 3. 0.3 mg/kg BW AFB<sub>1</sub> + 100 mg/kg BW EGCG (AFB<sub>1</sub> + EGCG); 4. 0.3 mg/kg BW AFB<sub>1</sub> + 30 mg/kg BW GSH (AFB<sub>1</sub> + GSH); 5. 0.3 mg/kg BW AFB<sub>1</sub> + 100 mg/kg BW EGCG + 30 mg/kg BW GSH (AFB<sub>1</sub> + EGCG + GSH). The experiment lasted for seven days. Compared with the CTR group, AFB<sub>1</sub> reduced 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. AFB<sub>1</sub> 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 AFB<sub>1</sub>-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 AFB<sub>1</sub> by inhibiting oxidative stress and attenuating excessive mitochondria-mediated apoptosis.https://www.mdpi.com/2072-6651/14/12/876aflatoxin B<sub>1</sub>ducklingepigallocatechin gallateglutathioneoxidative stressKeap1/Nrf2 signalling |
| spellingShingle | Yanan Wang Jiayu Wu Lingfeng Wang Ping Yang Zuhong Liu Shahid Ali Rajput Mubashar Hassan Desheng Qi Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway Toxins aflatoxin B<sub>1</sub> duckling epigallocatechin gallate glutathione oxidative stress Keap1/Nrf2 signalling |
| title | Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway |
| title_full | Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway |
| title_fullStr | Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway |
| title_full_unstemmed | Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway |
| title_short | Epigallocatechin Gallate and Glutathione Attenuate Aflatoxin B<sub>1</sub>-Induced Acute Liver Injury in Ducklings via Mitochondria-Mediated Apoptosis and the Nrf2 Signalling Pathway |
| title_sort | epigallocatechin gallate and glutathione attenuate aflatoxin b sub 1 sub induced acute liver injury in ducklings via mitochondria mediated apoptosis and the nrf2 signalling pathway |
| topic | aflatoxin B<sub>1</sub> duckling epigallocatechin gallate glutathione oxidative stress Keap1/Nrf2 signalling |
| url | https://www.mdpi.com/2072-6651/14/12/876 |
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