Soybean β-conglycinin caused intestinal inflammation and oxidative damage in association with NF-κB, TOR and Nrf2 in juvenile grass carp (Ctenopharyngodon idella): varying among different intestinal segments

The current study aimed to investigate the effects and mechanisms of dietary soybean beta-conglycinin in immune function and oxidative damage among different intestinal segments of juvenile grass carp (Ctenopharyngodon idella). 240 fish (13.77 +/- 0.10 g) were fed control or 8% 13-conglycinin diet for 7 weeks. Dietary beta-conglycinin caused inconsistent suppression effects on the innate immune by decreasing complement component, lysozyme, antimicrobial peptide and acid phosphatase among different intestinal segments. Meanwhile, dietary beta-conglycinin caused inflammation in the mid and distal intestine by raising pro -inflammatory cytokines and declining antiinflammatory cytokines mRNA levels, while more serious in the distal intestine than in the mid intestine. Furthermore, dietary beta-conglycinin regulating inflammatory cytokines might be associated with transcription factors nuclear factor-kappa B P65 (NF-KB P65) nucleus translocation and target of rapamycin (TOR) phosphorylation in the distal intestine but only related to TOR phosphorylation in the mid intestine. Interestingly, in the proximal intestine, dietary beta-conglycinin decreased both pro-inflammatory and anti-inflammatory cytokines mRNA level, and did not affect NF-x13 P65 nucleus translocation and TOR phosphorylation. For oxidative damage, dietary beta-conglycinin exposure elevated both malondialdehyde (MDA) and protein carbonyl (PC) contents in the distal intestine, which might be attributed to the suppression of the Mn-SOD, catalase (CAT) and glutathione peroxidase (GPx) activities. In the mid intestine, dietary beta-conglycinin only increased PC content in association with the low activities of CAT, GPx and glutathione peroxidase (GR). Unexpectedly, in the proximal intestine, dietary beta-conglycinin did not significantly change MDA and PC contents while decreased antioxidant enzyme activities. Furtherly, dietary beta-conglycinin affect the antioxidant enzyme activity might be regulated by the varying pattern of nuclear factor-erythroid 2-related factor 2 (Nrf2) nucleus translocation among these three intestinal segments. In summary, dietary beta-conglycinin caused intestinal inflammation and oxidative damage in association with NF-kappa B, TOR and Nrf2 signaling molecules, which were varying among the three intestinal segments of grass carp.