No abstract

The alleviating effect of Sodium butyrate (SB) on intestinal injuries incurred by glycinin in feed was investigated in common carp. The control group (without glycinin and SB), the Gly group (with 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 findings revealed that glycinin caused apoptosis in the intestine, up-regulated JNK, caspase-3, Bax, caspase-9, p38, caspase-8 and FasL gene expression in the MI, DI and hepatopancreas, while down-regulating ERK and Bcl-2 apoptotic genes. However, no eminent effect on the PI. In contrast, SB2 and SB3 groups eminently reversed these adverse effects. Dietary glycinin eminently reduced the expression of ZO-1, Claudin3, Claudin7 and Occludin1 genes in the MI and DI. SB2 and SB3 groups eminently up-regulated the expression of ZO-1, Claudin3, Claudin7 and Occludin1 expression levels, thereby improving the function of the tightly connected barrier in the intestine. Dietary glycinin also eminently increased serum levels of D-lactate, diamine oxidase, serotonin and endothelin, leading to intestinal damage and increased intestinal permeability. SB2 and SB3 groups reduced serum levels of D-lactate, diamine oxidase, serotonin and endothelin, regulating intestinal permeability. Glycinin disrupted the morphological structure of the intestine, while the SB2 and SB3 groups increased the height and width of the folds of the intestinal villi, thus maintaining the morphological integrity of the intestine. Dietary glycinin upset the intestinal microecological balance by increasing Proteobacteria abundance while lowering Clostridium and Bacteroidetes abundance. The SB2 and SB3 groups altered the composition and number of dominant taxa while increasing the abundance of Firmicutes and Acidobacteria. In conclusion, SB could inhibit apoptosis of intestinal cells through the JNK/FasL/caspase-8 signalling pathway and up-regulate the expression of intestinal tight junction (TJ) genes, maintain intestinal physical barrier and regulate intestinal flora, thereby alleviating glycinin-induced intestinal damage.

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.