Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways
Difenoconazole (DFZ) is a classical triazole fungicide that causes immunosuppression in non-target organisms. Ferulic acid (FA) is a polyphenolic molecule found in nature that has antioxidant and anti-inflammatory activities. The purpose of this investigation was to see if FA could prevent DFZ-induc...
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| 格式: | 文件 |
| 语言: | English |
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Elsevier
2023-09-01
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| 丛编: | Ecotoxicology and Environmental Safety |
| 主题: | |
| 在线阅读: | http://www.sciencedirect.com/science/article/pii/S0147651323008436 |
| _version_ | 1827866514927124480 |
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| author | Haoming Ma Zihui Meng Li Zhou Huimiao Feng Xinyu Wu Yue Xin Jingquan Dong Yanan Li |
| author_facet | Haoming Ma Zihui Meng Li Zhou Huimiao Feng Xinyu Wu Yue Xin Jingquan Dong Yanan Li |
| author_sort | Haoming Ma |
| collection | DOAJ |
| description | Difenoconazole (DFZ) is a classical triazole fungicide that causes immunosuppression in non-target organisms. Ferulic acid (FA) is a polyphenolic molecule found in nature that has antioxidant and anti-inflammatory activities. The purpose of this investigation was to see if FA could prevent DFZ-induced immunosuppression and to identify the potential mechanisms. Carp were exposed to 1/10 LC50 of DFZ as well as fed normal feed or feed containing dietary additive FA for 30 d. It was found that DFZ-induced immunosuppression could be improved by FA, as evidenced by upregulation of Hb, C3 and IgM and downregulation of LDH. It was then investigated that FA could ameliorate DFZ-induced splenic injury through p53-mediated apoptosis. At the same time, enhancing the levels of CAT, GSH and T-AOC in spleen and transcription levels Nrf2 signaling pathway related genes indicated that FA reduced oxidative damage caused by DFZ by blocking the Nrf2 signaling pathway. In addition, FA inhibited the inflammatory response triggered by TRAF/TAK1/NF-κB signaling pathway, downregulated the transcript levels of pro-inflammatory factors (il-1β, tnf-α, il-6) and the level of NLRP3 inflammasome (NRLP3, ASC, Caspase 1), and upregulated the transcript levels of anti-inflammatory factors (tgf-β1, il-10). In conclusion, the above results suggested that FA mediated TRAF/TAK1/NF-κB, Nrf2, and p53 pathways to attenuate DFZ-induced inflammation, oxidative stress, and apoptosis thereby enhancing the immune capacity of carp. |
| first_indexed | 2024-03-12T15:05:46Z |
| format | Article |
| id | doaj.art-d6f04bf722714e25b13acabab09a826a |
| institution | Directory Open Access Journal |
| issn | 0147-6513 |
| language | English |
| last_indexed | 2024-03-12T15:05:46Z |
| publishDate | 2023-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj.art-d6f04bf722714e25b13acabab09a826a2023-08-13T04:52:07ZengElsevierEcotoxicology and Environmental Safety0147-65132023-09-01262115339Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathwaysHaoming Ma0Zihui Meng1Li Zhou2Huimiao Feng3Xinyu Wu4Yue Xin5Jingquan Dong6Yanan Li7Jiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, China; School of Food Science and Pharmaceutical Engineering, Nanjing Normal University, Nanjing 210023, ChinaSchool of Food Science and Pharmaceutical Engineering, Nanjing Normal University, Nanjing 210023, ChinaSchool of Food Science and Pharmaceutical Engineering, Nanjing Normal University, Nanjing 210023, ChinaJiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, ChinaJiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, ChinaJiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, ChinaJiangsu Key Laboratory of Marine Bioresources and Environment, Co-Innovation Center of Jiangsu Marine Bio-industry Technology, Jiangsu Key Laboratory of Marine Pharmaceutical Compound Screening, Jiangsu Ocean University, Lianyungang 222005, China; Corresponding authors.School of Food Science and Pharmaceutical Engineering, Nanjing Normal University, Nanjing 210023, China; Corresponding authors.Difenoconazole (DFZ) is a classical triazole fungicide that causes immunosuppression in non-target organisms. Ferulic acid (FA) is a polyphenolic molecule found in nature that has antioxidant and anti-inflammatory activities. The purpose of this investigation was to see if FA could prevent DFZ-induced immunosuppression and to identify the potential mechanisms. Carp were exposed to 1/10 LC50 of DFZ as well as fed normal feed or feed containing dietary additive FA for 30 d. It was found that DFZ-induced immunosuppression could be improved by FA, as evidenced by upregulation of Hb, C3 and IgM and downregulation of LDH. It was then investigated that FA could ameliorate DFZ-induced splenic injury through p53-mediated apoptosis. At the same time, enhancing the levels of CAT, GSH and T-AOC in spleen and transcription levels Nrf2 signaling pathway related genes indicated that FA reduced oxidative damage caused by DFZ by blocking the Nrf2 signaling pathway. In addition, FA inhibited the inflammatory response triggered by TRAF/TAK1/NF-κB signaling pathway, downregulated the transcript levels of pro-inflammatory factors (il-1β, tnf-α, il-6) and the level of NLRP3 inflammasome (NRLP3, ASC, Caspase 1), and upregulated the transcript levels of anti-inflammatory factors (tgf-β1, il-10). In conclusion, the above results suggested that FA mediated TRAF/TAK1/NF-κB, Nrf2, and p53 pathways to attenuate DFZ-induced inflammation, oxidative stress, and apoptosis thereby enhancing the immune capacity of carp.http://www.sciencedirect.com/science/article/pii/S0147651323008436Ferulic acidDifenoconazoleOxidative stressInflammationApoptosis |
| spellingShingle | Haoming Ma Zihui Meng Li Zhou Huimiao Feng Xinyu Wu Yue Xin Jingquan Dong Yanan Li Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways Ecotoxicology and Environmental Safety Ferulic acid Difenoconazole Oxidative stress Inflammation Apoptosis |
| title | Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways |
| title_full | Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways |
| title_fullStr | Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways |
| title_full_unstemmed | Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways |
| title_short | Ferulic acid attenuated difenoconazole-induced immunotoxicity in carp by inhibiting TRAF/TAK1/NF-κB, Nrf2 and p53 pathways |
| title_sort | ferulic acid attenuated difenoconazole induced immunotoxicity in carp by inhibiting traf tak1 nf κb nrf2 and p53 pathways |
| topic | Ferulic acid Difenoconazole Oxidative stress Inflammation Apoptosis |
| url | http://www.sciencedirect.com/science/article/pii/S0147651323008436 |
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