Yeast culture improve CCl ₄ ‐induced liver damage, inflammatory response via inhibition of TLR2/NF‐kB signaling pathway expression in Pseudobagrus ussuriensis

Abstract

The aim of this study was to investigate the underlying hepatoprotective effects of yeast culture (YC) against carbon tetrachloride (CCl 4 )-induced hepatic damage in Pseudobagrus ussuriensis. The fish were randomly divided into three experimental groups (Control, CCl 4 and YC+CCl 4 ) with three replicates of 30 fish in each replicate.Firstly, the Control and CCl 4 groups were fed basal diet without yeast culture, and the YC+CCl 4 group was fed diet with 20 g/kg YC for 8 weeks. After the end of feeding experiment, Control group was intraperitoneally injected olive oil with 0.05 ml/15 g fish body weight, while CCl 4 and YC+CCl 4 groups were intraperitoneally injected CCl 4 olive oil solution (CCl 4 : olive oil = 3:7) with 0.05 ml/15 g fish body weight for 48 h. The results indicated that fish fed with 20 g/kg yeast culture not only ameliorated injured hepatic cell, as evidenced by well-preserved liver architecture, but also significantly decreased plasma AST activity in the CCl 4 -induced hepatic injury model. Next, we found that dietary 20 g/kg YC supplementation could improve hepatic antioxidant activity and inhibit lipid peroxidation induced by CCl 4 . Fish fed 20 g/kg YC could suppress the decrease of plasma IgM and plasma ACH50 content caused by CCl 4 (p < .05).In addition, we also found that fish treated with CCl 4 up-regulated the expression of immune-related genes (TLR2, MyD88 and NF-κBp65), proinflammatory cytokines (IL-1β and IL-8) and Hsp70 mRNA expression in liver compared with the Control group; meanwhile, fish fed with 20 g/kg YC down-regulated the above-mentioned genes expressions in liver compared with CCl 4 group. In general, the results mentioned above suggested that the dietary yeast culture could relieve the oxidative stress, immune damage and liver injury induced by CCl 4 and could also suppress CCl 4 -induced inflammation through inhibiting the TLR2/NF-κB signalling pathway.