The aim of this study was to investigate the effects of aspirin eugenol ester (AEE) on liver oxidative damage and energy metabolism in immune-stressed broilers. In total, 312 broilers were divided into 4 groups (saline, LPS, SAEE, and LAEE). Broilers in the saline and LPS groups were fed a basal diet; the SAEE and LAEE groups had an added 0.01% AEE in their diet. Broilers in the LPS and LAEE groups were injected with lipopolysaccharides, while the saline and SAEE groups were injected with saline. Results showed that AEE increased the body weight, average daily gain, and average daily feed intake, as well as decreasing the feed conversion ratio of immune-stressed broilers. AEE protects against oxidative damage in immune-stressed broiler livers by elevating the total antioxidant capacity, superoxide dismutase activity, and glutathione S-transferase alpha 3 (GSTA3) and glutaredoxin 2 (GLRX2) expression, while decreasing malondialdehyde content. AEE lessened inflammation by reducing prostaglandin-F2α production and prostaglandin-endoperoxide synthase 2 (PTGS2) and interleukin-1beta (IL-1β) expression. AEE decreased oxidative phosphorylation rates by increasing succinic acid levels and lowering both adenosine diphosphate (ADP) levels and ceroid lipofuscinosis neuronal 5 (CLN5) expression. AEE modulated the metabolism of phenylalanine, tyrosine, lipids, and cholesterol by reducing the phenyllactate and L-arogenate levels, lowering dopachrome tautomerase (DCT) and apolipoprotein A4 (APOA4) expression, and increasing phenylpyruvic acid and dopa decarboxylase (DDC) expression. In summary, AEE can effectively alleviate liver oxidative damage and energy metabolism disorders in immune-stressed broilers.

This study investigated the influence of dietary aspirin eugenol ester (AEE) on growth performance, ileum antioxidant capacity, intestinal barrier function and ileum microbiota of broilers subjected to high stocking density stress (HDS). A total of 360 one-day-old Arbor Acres broilers were randomly assigned to four treatment groups: normal density (ND, 14 broilers/m²), normal density + AEE (NDAEE), high density (HD, 22 broilers/m²) and high density + AEE (HDAEE). HDS leads to a significant decrease in broiler performance while reducing the antioxidant capacity of the gut. Morphologic examination of the intestine revealed that HDS causes damage to the intestinal villi. Dietary addition of AEE significantly increased body weight gain and improved antioxidant capacity with restoration of intestinal morphology in broilers with HDS. In addition, HDS resulted in decreased gene expression of ileum tight junction proteins and significantly increased gene expression of inflammatory factors in broilers. Dietary addition of AEE effectively alleviated the decrease in tight junction protein gene expression in broilers with HDS and reduced the expression of HDS-induced inflammatory cytokines through the COX-2-mPGES-1 signaling pathway. AEE supplementation improved microbiota diversity and increased the relative abundance of Lactobacillus and Ileibacterium. Thus, dietary AEE effectively reduced the negative effects of HDS on productivity, gut microbiota and overall health in broilers and could be a worthwhile dietary supplement for offsetting negative effects of stocking stress in broilers.

The global poultry industry faces escalating challenges in animal welfare and production efficiency in the post-antibiotic era. Feed intake, a crucial determinant of growth, is frequently suppressed under stress, forming a key bottleneck for sustainable production. The microbiota–gut–brain (MGB) axis provides a novel framework to understand this complex regulation. Short-chain fatty acids (SCFAs), produced from dietary fiber by gut microbiota, serve as vital chemical messengers within this axis, modulating hypothalamic feeding centers and systemic metabolism. This review summarizes SCFA biosynthesis and kinetics in poultry and examines their neural, humoral, and immune pathways to the brain. Emphasis is placed on receptor-mediated signaling, epigenetic regulation, energy sensing, and neuroimmune modulation through which SCFAs regulate feeding and reduce inflammation. Practical strategies—such as substrate engineering, microbiota modulation, and exogenous regulators—are discussed to enhance SCFA levels and poultry health. Future directions include multi-omics integration, novel additives, and predictive models to advance antibiotic-free nutrition.

This study evaluated whether chlorogenic acid (CGA) attenuates hepatic injury in broilers under high stocking density (HSD). A total of 216 experimental male Arbor Acres broilers were assigned to normal density without CGA (ND; 14 birds/m²), high density without CGA (HD; 22 birds/m²), normal density with 0.1% CGA (NDCGA), or high density with 0.1% CGA (HDCGA) groups, with six cages per treatment. CGA was supplied from day 7 to 42. At 42 d, live-weight densities were 35.00, 50.25, 34.48, and 49.38 kg/m², respectively. Compared with their corresponding normal-density groups, the high-density groups had lower body weights at 21, 28, 35, and 42 d, and lower average daily gain (ADG) during days 21–42 (p < 0.05), whereas CGA did not significantly alter body weight or ADG within either stocking density (p > 0.05). At 35 and 42 d, the HD group had lower hepatic T-AOC, SOD, and CAT activities and higher MDA content than the ND group (p < 0.05). Compared with the HD group, the HDCGA group had higher T-AOC and CAT activities and lower MDA content at both ages, and higher SOD activity at 42 d (p < 0.05). Qualitative histological and transcript-level alterations were evident at 28 d. Compared with HD, the HDCGA group showed treatment-associated shifts in AMPK, SREBP1, ACACA, PLA2G4A, COX-2, ALOX5, and NOX5 mRNA abundance (p < 0.05). Under the experimental conditions, 0.1% CGA was associated with partial attenuation of HSD-related hepatic oxidative, lipid-metabolic, and inflammatory disturbances without a significant growth response.