The mycotoxin zearalenone (ZEA) in food and feed seriously harms human and animal health. How to reduce its toxicity is an important direction of current research on food safety. This study aim to assess the effects of procyanidins (PC) on cell apoptosis caused by ZEA and to clarify the role of Nrf2 in the process. Swine testicle (ST) cells were treated with ZEA (57.5 μmol/L) and/or PC (10 mg/L) for 24 h. Cell viability was detected by CCK-8 assay. Cell apoptosis and the level of ROS were detected by flow cytometry. The expression levels of mRNA and protein was detected by qRT-PCR and western blotting. Our results showed that ZEA reduced the antioxidant capacity of the ST cells, induced the cell apoptosis and inhibited the gene and protein expression of Nrf2 and its downstream genes (ho-1,nqo1), while PC improved the cell antioxidant capacity, reduced the degree of ZEA-induced cell apoptosis and promoted the gene and protein expression of Nrf2 and its downstream genes. However, when the Nrf2 small molecule inhibitor ML385 was added, the ability of PC to inhibit ZEA-induced cell apoptosis and promote the expression of Nrf2 and its downstream genes were decreased. Our results demonstrated that ZEA induced oxidative stress and apoptosis of ST cells, which were alleviated by PC intervention via activating Nrf2 signaling pathway. This finding of this study provided a molecular basis for the clinical application of PC to prevent ZEN-caused reproductive toxicity.

Biomedical Research Center University Hospital Hradec Kralove Hradec Kralove Czech Republic

Department of Chemistry Faculty of Science University of Hradec Kralove 50003 Hradec Kralove Czech Republic

Key Laboratory of Livestock Infectious Diseases Ministry of Education College of Animal Science and Veterinary Medicine Shenyang Agricultural University Shenyang 110866 China

MOE Joint International Research Laboratory of Animal Health and Food Safety College of Veterinary Medicine Nanjing Agricultural University Nanjing 210095 China

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$a Yan, Rong $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China

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$a Procyanidins inhibit zearalenone-induced apoptosis and oxidative stress of porcine testis cells through activation of Nrf2 signaling pathway / $c R. Yan, H. Wang, J. Zhu, T. Wang, E. Nepovimova, M. Long, P. Li, K. Kuca, W. Wu

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$a The mycotoxin zearalenone (ZEA) in food and feed seriously harms human and animal health. How to reduce its toxicity is an important direction of current research on food safety. This study aim to assess the effects of procyanidins (PC) on cell apoptosis caused by ZEA and to clarify the role of Nrf2 in the process. Swine testicle (ST) cells were treated with ZEA (57.5 μmol/L) and/or PC (10 mg/L) for 24 h. Cell viability was detected by CCK-8 assay. Cell apoptosis and the level of ROS were detected by flow cytometry. The expression levels of mRNA and protein was detected by qRT-PCR and western blotting. Our results showed that ZEA reduced the antioxidant capacity of the ST cells, induced the cell apoptosis and inhibited the gene and protein expression of Nrf2 and its downstream genes (ho-1,nqo1), while PC improved the cell antioxidant capacity, reduced the degree of ZEA-induced cell apoptosis and promoted the gene and protein expression of Nrf2 and its downstream genes. However, when the Nrf2 small molecule inhibitor ML385 was added, the ability of PC to inhibit ZEA-induced cell apoptosis and promote the expression of Nrf2 and its downstream genes were decreased. Our results demonstrated that ZEA induced oxidative stress and apoptosis of ST cells, which were alleviated by PC intervention via activating Nrf2 signaling pathway. This finding of this study provided a molecular basis for the clinical application of PC to prevent ZEN-caused reproductive toxicity.

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$a Wang, Hanli $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China

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$a Zhu, Jiangning $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China

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$a Wang, Tiancheng $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China

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$a Nepovimova, Eugenie $u Department of Chemistry, Faculty of Science, University of Hradec Kralove, 50003, Hradec Kralove, Czech Republic

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$a Long, Miao $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China. Electronic address: longmiao@syau.edu.cn

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$a Li, Peng $u Key Laboratory of Livestock Infectious Diseases, Ministry of Education, College of Animal Science & Veterinary Medicine, Shenyang Agricultural University, Shenyang, 110866, China. Electronic address: lipeng2008@syau.edu.cn

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$a Kuca, Kamil $u Department of Chemistry, Faculty of Science, University of Hradec Kralove, 50003, Hradec Kralove, Czech Republic; Biomedical Research Center, University Hospital Hradec Kralove, Hradec Kralove, Czech Republic. Electronic address: kamil.kuca@uhk.cz

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$a Wu, Wenda $u MOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China; Department of Chemistry, Faculty of Science, University of Hradec Kralove, 50003, Hradec Kralove, Czech Republic. Electronic address: wuwenda@njau.edu.cn

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