Potential protective effects of sodium butyrate on glycinin-induced oxidative stress, inflammatory response and growth inhibition in Cyprinus carpio

Abstract

Investigated mitigating effects of sodium butyrate (SB) on the inflammatory response, oxidative stress and growth inhibition of common carp (2.94 ± 0.2 g) caused by dietary glycinin. The control group (without glycinin and SB), Gly group (contain glycinin), and the remaining 4 groups were added SB (0.75, 1.50, 2.25, 3.00 g/kg,) respectively based on the Gly group. 6 groups of diets were isonitrogenous and isoenergetic, and fish were fed with these 6 diets for eight weeks. The reduction of FBW, FER, SGR, WGR and PER of common carp caused by dietary glycinin could be significantly improved by supplementing 1.50–2.25 g/kg SB in the diet, but FBW, WGR and SGR did not reach the level of the control group. Hepatopancreas and intestinal protease activities and the content of muscle crude protein were significantly decreased by dietary glycinin, but supplement 1.50–2.25 g/kg SB partially reversed this result. Supplementation with 1.50–2.25 g/kg SB not only raised AST and ALT activities in hepatopancreas but also decreased AST and ALT activities in serum. Glycinin significantly reduced immune and antioxidant enzyme activities, in contrast, supplementation of 1.50–2.25 g/kg SB reversed these adverse effects. Furthermore, compared with the Gly group, supplement 1.50–2.25 g/kg SB eminently up-regulated the TGF-β and IL-10 mRNA, and down-regulated the IL-1β, TNF-α, and NF-κB mRNA in hepatopancreas, mid intestine (MI) and distal intestine (DI). Meanwhile, supplement 1.50–2.25 g/kg SB activated the Keap1-Nrf2-ARE signalling pathway, and upregulate CAT, SOD and HO-1 mRNA expression in hepatopancreas, MI and DI. Summarily, glycinin significantly decreased the digestive function and induced inflammatory response, and oxidative stress of common carp ultimately inducing growth inhibition. However, SB partially mitigated these adverse effects by activating the Keap1-Nrf2-ARE signalling pathway and inhibiting the NF-κB signalling pathway.