COS Attenuates AFB1-Induced Liver Injury in Medaka through Inhibition of Histopathological Damage and Oxidative Stress

Abstract

Aflatoxin B1 (AFB1) –induced liver damage may be treated with chitosan oligosaccharide (COS), a small-molecular–weight oligosaccharide with excellent bioactivity and antioxidant potential. Hepatotoxicity induced by AFB1 single acute exposure (ASAE) has been theoretically established but the mechanism of toxicity in aquatic models has been less studied. In this paper, a model of liver injury in Japanese medaka (Oryzias latipes) after ASAE for 72 h and a model of liver injury healing after ASAE following a COS intervention for 72 h were developed. The different effects of ASAE and COS interventions for ASAE were analyzed at the phenotypic and genetic levels. The results showed that AFB1 reduced body weight and hepatopancreatic somatic indices (HSI) in medaka. Moreover, AFB1–induced histopathological damage and oxidative stress injury were concentration–dependent but the symptoms of damage were attenuated to some extent by the addition of the intervention drug COS, and the intervention effect of high concentrations of COS was almost identical to silymarin (SIL). Using the RNA–Seq technique, COS reduces the number of differentially expressed genes (DEGs) brought about by AFB1. Among the genes associated with tumors, hepatocellular carcinoma and hepatitis aurka, thbs1, serpine1, fabp7, and dusp5 were also validated by Q-PCR with corresponding trends. In conclusion, AFB1 can cause liver injury in medaka and COS has a therapeutic effect, and these impacted genes have the potential to become therapeutic targets for COS intervention in AFB1–induced liver disease.