Chen Lin, Yan Jiahui, Shi Huijun, Zhang Zhaohuan, Zhao YueLiang, Zhao Yong, Wang Yuan, Ou Jie
College of Food Sciences and Technology, Shanghai Ocean University, Shanghai, 201306, China.
Shanghai Engineering Research Center of Aquatic Product Processing and Preservation, Shanghai, 201306, China.
Bioresour Bioprocess. 2024 Jan 18;11(1):13. doi: 10.1186/s40643-023-00708-6.
Aflatoxin B (AFB) 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 AFB-induced acute liver injury. In this study, rats were acutely exposed to 1 mg/kg BW AFB 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, AFB-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 AFB on hepatic genes and thus reduces the changes in hepatic gene function.
黄曲霉毒素B（AFB）具有极强的肝毒性，是肝癌的致病因子，可引发急性或慢性肝损伤症状。壳寡糖（COS）由虾蟹壳来源的壳聚糖降解得到，是一种天然抗氧化物质，其抗肿瘤特性已得到广泛研究，但关于预防AFB诱导的急性肝损伤的研究较少。在本研究中，大鼠急性暴露于1 mg/kg体重的AFB，并同时灌胃不同剂量的COS，持续8天。结果表明，COS减轻了大鼠肝脏组织病理学变化，降低了血清生化指标（ALT、AST、ALP和TBIL）。它显著抑制了MDA含量，促进了SOD和GSH-Px活性的产生。此外，它还改善了肝细胞凋亡。此外，AFB与高剂量COS差异基因富集了622个GO条目，其中380个是生物过程，170个是分子功能，72个是细胞成分。通过KEGG富集分析的差异表达基因（DEG）在代谢、PPAR信号通路和过氧化物酶体等途径中富集程度更高。Q-PCR技术验证了DEG中的Lama5、Egr1、Cyp2b1和Gadd45g与氧化应激损伤和凋亡相关。总之，COS干预降低了AFB对肝脏基因的影响，从而减少了肝脏基因功能的变化。
