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Intervention mechanism of marine-based chito-oligosaccharide on acute liver injury induced by AFB1 in rats.
Chen, Lin; Yan, Jiahui; Shi, Huijun; Zhang, Zhaohuan; Zhao, YueLiang; Zhao, Yong; Wang, Yuan; Ou, Jie.
Affiliation
  • Chen L; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • Yan J; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • Shi H; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • Zhang Z; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • Zhao Y; Shanghai Engineering Research Center of Aquatic Product Processing and Preservation, Shanghai, 201306, China.
  • Zhao Y; Laboratory of Quality and Safety Risk Assessment for Aquatic Product on Storage and Preservation, Ministry of Agriculture and Rural Affairs, Shanghai, 201306, China.
  • Wang Y; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
  • Ou J; College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
Bioresour Bioprocess ; 11(1): 13, 2024 Jan 18.
Article in En | MEDLINE | ID: mdl-38647922
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.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Bioresour Bioprocess Year: 2024 Document type: Article Affiliation country: China

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: Bioresour Bioprocess Year: 2024 Document type: Article Affiliation country: China