Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats
Abstract Aflatoxin B1 (AFB1) is extremely hepatotoxic, a causative agent of liver cancer, and can cause symptoms of acute or chronic liver damage. Chito-oligosaccharides (COS), obtained from the degradation of chitosan derived from shrimp and crab shells, is a natural antioxidant substance and its a...
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SpringerOpen
2024-01-01
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Series: | Bioresources and Bioprocessing |
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Online Access: | https://doi.org/10.1186/s40643-023-00708-6 |
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author | Lin Chen Jiahui Yan Huijun Shi Zhaohuan Zhang YueLiang Zhao Yong Zhao Yuan Wang Jie Ou |
author_facet | Lin Chen Jiahui Yan Huijun Shi Zhaohuan Zhang YueLiang Zhao Yong Zhao Yuan Wang Jie Ou |
author_sort | Lin Chen |
collection | DOAJ |
description | Abstract Aflatoxin B1 (AFB1) is extremely hepatotoxic, a causative agent of liver cancer, and can cause symptoms of acute or chronic liver damage. Chito-oligosaccharides (COS), obtained from the degradation of chitosan derived from shrimp and crab shells, is a natural antioxidant substance and its antitumor properties have been widely studied, but less research has been done on the prevention of AFB1-induced acute liver injury. In this study, rats were acutely exposed to 1 mg/kg BW AFB1 and simultaneously gavaged with different doses of COS for 8 days. The results showed that COS attenuated the hepatic histopathological changes and reduced serum biochemical indices (ALT, AST, ALP, and TBIL) in rats. It significantly inhibited MDA content and promoted SOD and GSH-Px activity production. Moreover, it also improved hepatocyte apoptosis. Furthermore, AFB1-vs-HCOS differential genes were enriched with 622 GO entries, and 380 were Biological Processes, 170 were Molecular Functions, 72 were Cellular Components. Differentially expressed genes (DEGs) analyzed by KEGG enrichment were more enriched in pathways, such as metabolism, PPAR signaling pathway, and peroxisome. Q-PCR technique verified that Lama5, Egr1, Cyp2b1, and Gadd45g in DEGs were associated with oxidative stress damage and apoptosis. In conclusion, COS intervention reduces the effect of AFB1 on hepatic genes and thus reduces the changes in hepatic gene function. Graphical abstract |
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issn | 2197-4365 |
language | English |
last_indexed | 2024-03-08T12:41:34Z |
publishDate | 2024-01-01 |
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spelling | doaj.art-aa21d2d8aa4a48bc9c1cb4473d8531a62024-01-21T12:08:22ZengSpringerOpenBioresources and Bioprocessing2197-43652024-01-0111111310.1186/s40643-023-00708-6Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in ratsLin Chen0Jiahui Yan1Huijun Shi2Zhaohuan Zhang3YueLiang Zhao4Yong Zhao5Yuan Wang6Jie Ou7College of Food Sciences and Technology, Shanghai Ocean UniversityCollege of Food Sciences and Technology, Shanghai Ocean UniversityCollege of Food Sciences and Technology, Shanghai Ocean UniversityCollege of Food Sciences and Technology, Shanghai Ocean UniversityCollege of Food Sciences and Technology, Shanghai Ocean UniversityCollege of Food Sciences and Technology, Shanghai Ocean UniversityEngineering Research Center of Modern Preparation Technology of TCM, Shanghai University of Traditional Chinese MedicineCollege of Food Sciences and Technology, Shanghai Ocean UniversityAbstract Aflatoxin B1 (AFB1) is extremely hepatotoxic, a causative agent of liver cancer, and can cause symptoms of acute or chronic liver damage. Chito-oligosaccharides (COS), obtained from the degradation of chitosan derived from shrimp and crab shells, is a natural antioxidant substance and its antitumor properties have been widely studied, but less research has been done on the prevention of AFB1-induced acute liver injury. In this study, rats were acutely exposed to 1 mg/kg BW AFB1 and simultaneously gavaged with different doses of COS for 8 days. The results showed that COS attenuated the hepatic histopathological changes and reduced serum biochemical indices (ALT, AST, ALP, and TBIL) in rats. It significantly inhibited MDA content and promoted SOD and GSH-Px activity production. Moreover, it also improved hepatocyte apoptosis. Furthermore, AFB1-vs-HCOS differential genes were enriched with 622 GO entries, and 380 were Biological Processes, 170 were Molecular Functions, 72 were Cellular Components. Differentially expressed genes (DEGs) analyzed by KEGG enrichment were more enriched in pathways, such as metabolism, PPAR signaling pathway, and peroxisome. Q-PCR technique verified that Lama5, Egr1, Cyp2b1, and Gadd45g in DEGs were associated with oxidative stress damage and apoptosis. In conclusion, COS intervention reduces the effect of AFB1 on hepatic genes and thus reduces the changes in hepatic gene function. Graphical abstracthttps://doi.org/10.1186/s40643-023-00708-6Aflatoxin B1Chito-oligosaccharideOxidative StressApoptosisRNA-Seq |
spellingShingle | Lin Chen Jiahui Yan Huijun Shi Zhaohuan Zhang YueLiang Zhao Yong Zhao Yuan Wang Jie Ou Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats Bioresources and Bioprocessing Aflatoxin B1 Chito-oligosaccharide Oxidative Stress Apoptosis RNA-Seq |
title | Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats |
title_full | Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats |
title_fullStr | Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats |
title_full_unstemmed | Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats |
title_short | Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats |
title_sort | intervention mechanism of marine based chito oligosaccharide on acute liver injury induced by afb1 in rats |
topic | Aflatoxin B1 Chito-oligosaccharide Oxidative Stress Apoptosis RNA-Seq |
url | https://doi.org/10.1186/s40643-023-00708-6 |
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