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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Main Authors: Lin Chen, Jiahui Yan, Huijun Shi, Zhaohuan Zhang, YueLiang Zhao, Yong Zhao, Yuan Wang, Jie Ou
Format: Article
Language:English
Published: SpringerOpen 2024-01-01
Series:Bioresources and Bioprocessing
Subjects:
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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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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