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

• Published in: Fish & shellfish immunology 2019-12, Vol.95, p.105-116
• Main Authors: Duan, Xu-Dong, Jiang, Wei-Dan, Wu, Pei, Liu, Yang, Jiang, Jun, Tan, Bei-Ping, Yang, Qi-Hui, Kuang, Sheng-Yao, Tang, Ling, Zhou, Xiao-Qiu, Feng, Lin
• Format: Article
• Language: English
• Subjects: Animal Feed - adverse effects; Animals; Antigens, Plant - adverse effects; Carps - genetics; Carps - immunology; Dietary Supplements - adverse effects; Fish Proteins - genetics; Fish Proteins - immunology; Globulins - adverse effects; Grass carp (Ctenopharyngodon idella); Immune; Immunity, Innate; Inflammation; Intestinal segment; Intestines - pathology; NF-E2-Related Factor 2 - immunology; NF-kappa B - immunology; NF-κB; Nrf2; Oxidative damage; Oxidative Stress; Seed Storage Proteins - adverse effects; Signal Transduction; Soybean Proteins - adverse effects; TOR; TOR Serine-Threonine Kinases - immunology; β‐conglycinin
• ISSN: 1050-4648; 1095-9947
• DOI: 10.1016/j.fsi.2019.10.021

The current study aimed to investigate the effects and mechanisms of dietary soybean β-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% β‐conglycinin diet for 7 weeks. Dietary β-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 β-conglycinin caused inflammation in the mid and distal intestine by raising pro-inflammatory cytokines and declining anti-inflammatory cytokines mRNA levels, while more serious in the distal intestine than in the mid intestine. Furthermore, dietary β-conglycinin regulating inflammatory cytokines might be associated with transcription factors nuclear factor-κB P65 (NF-κB 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 β-conglycinin decreased both pro-inflammatory and anti-inflammatory cytokines mRNA level, and did not affect NF-κB P65 nucleus translocation and TOR phosphorylation. For oxidative damage, dietary β-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 β-conglycinin only increased PC content in association with the low activities of CAT, GPx and glutathione peroxidase (GR). Unexpectedly, in the proximal intestine, dietary β-conglycinin did not significantly change MDA and PC contents while decreased antioxidant enzyme activities. Furtherly, dietary β-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 β-conglycinin caused intestinal inflammation and oxidative damage in association with NF-κB, TOR and Nrf2 signaling molecules, which were varying among the three intestinal segments of grass carp. •β-conglycinin didn't induce proximal intestine inflammation and oxidative damage.•β-conglycinin-caused mid intestine inflammation related to TOR phosphorylation.•β-conglycinin-caused dista