Arabinoxylans (AX), the primary hemicellulose found in cereals and grasses, play a crucial role in regulating immunity, metabolism and various physiological processes, underscoring their value as essential components in dietary nutrition. Considering the extensive research on AX in piglet nutrition, this paper systematically reviews their impacts on gut health and microbiota in piglets, as well as the underlying mechanisms of action. AX have been shown to mediate gut barrier fortification through tight junction protein upregulation and orchestrate mucosal immunity homeostasis, consequently ameliorating early-weaning-associated diarrheal pathogenesis in piglets. Additionally, AX function as microbial ecological modulators through selective enrichment of beneficial commensal microbiota (e.g. Bifidobacterium spp. and Lactobacillus spp.), while simultaneously stimulating microbial biosynthesis of SCFA and ferulic acid exhibiting potent antioxidant and anti-inflammatory activity, thereby maintaining the intestinal health of piglets. This review offers valuable insights into their potential as a dietary intervention to support gut health and immune function in early-weaned piglets. However, most studies focus on single-source AX such as wheat or maize, with limited exploration of novel sources or comparative effects of source combinations. Future research should systematically investigate the molecular mechanisms of AX action, provide data-driven guidance for selecting AX sources in feed formulations and establish optimal inclusion levels in practical feeding regimens. Such efforts will further solidify the precision nutrition potential of AX in promoting sustainable and healthy growth in piglets.

An 8-week feeding experiment was conducted to investigate and confront the putative functions of chitosan (CTS) and chitooligosaccharide (COS) in the growth and homoeostasis of distal intestine in juvenile turbots fed diets containing soyabean meal (SBM). Three isolipidic and isonitrogenous diets were formulated by supplemented basal diet (based on a 400 g/kg SBM) with 7·5 g/kg CTS or with 2·0 g/kg COS. Our results indicated that both CTS and COS supplementation could significantly improve (i) the growth performance and feed efficiency ratio; (ii) antioxidant activity driven by metabolic enzymes (i.e. catalase, glutathione reductase, glutathione peroxidase and superoxide dismutase); (iii) glutathione levels; (iv) acid phosphatase and lysozyme activity and (v) IgM content. As a result, these two particular prebiotics were able to significantly attenuate the histological alterations due to local inflammation as well as to decrease the transcriptional levels of proinflammatory cytokines (i.e. IL-1β, IL-8 and TNF-α) and major pathway effectors (i.e. activator protein-1 (AP-1), NF-кB, p38 mitogen-activated protein kinase, c-Jun N-terminal kinase and extracellular regulated kinase). High-throughput sequencing data indicated that dietary CTS and COS could significantly decrease the diversity of intestinal bacteria but elevate the relative abundances of Bacillus, Lactobacillus and Pseudomonas genera. Altogether, these findings suggest that CTS and COS can improve growth of turbot, enhance intestinal immune and anti-oxidant systems and promote the balance of intestinal microbiota. The protective effects, elicited by these two prebiotics, against SBM-induced inflammation could be attributed to their roles in alleviating the overexpression of inflammatory cytokines by possibly down-regulating NF-кB, AP-1 and/or mitogen-activated protein kinases pathways.

The dietary flavonoid epicatechin has been reported to exhibit a wide range of biological activities. The objective of the present study was to investigate the time-dependent regulation by epicatechin on the activity of the main transcription factors (NF-κB, activator protein-1 (AP-1) and nuclear transcription factor erythroid 2p45-related factor (Nrf2)) related to antioxidant defence and survival and proliferation pathways in HepG2 cells. Treatment of cells with 10 μm-epicatechin induced the NF-κB pathway in a time-dependent manner characterised by increased levels of IκB kinase (IKK) and phosphorylated inhibitor of κB subunit-α (p-IκBα) and proteolytic degradation of IκB, which was consistent with an up-regulation of the NF-κB-binding activity. Time-dependent activation of the AP-1 pathway, in concert with enhanced c-Jun nuclear levels and induction of Nrf2 translocation and phosphorylation were also demonstrated. Additionally, epicatechin-induced NF-κB and Nrf2 were connected to reactive oxygen species intracellular levels and to the activation of cell survival and proliferation pathways, being phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) and extracellular regulated kinase (ERK) associated to Nrf2 modulation and ERK to NF-κB induction. These data suggest that the epicatechin-induced survival effect occurs by the induction of redox-sensitive transcription factors through a tight regulation of survival and proliferation pathways.