Oxidative stress increases the apoptosis of intestinal epithelial cells and impairs intestinal epithelial cell renewal, which further promotes intestinal barrier dysfunction and even death. Extensive evidence supports that resveratrol and apigenin have antioxidant, anti-inflammatory, and antiproliferative properties. Here, we investigated the ability of these two compounds to alleviate diquat-induced jejunal oxidative stress and morphological injury, using the duck as a model, as well as the effects of apigenin on oxidative stress induced by H₂O₂ in immortalized duck intestinal epithelial cells (IDECs). Ducks were randomly assigned to the following four groups, with five replicates: a control (CON) group, a diquat-challenged (DIQ) group, a resveratrol (500 mg/kg) + diquat (RES) group, and an apigenin (500 mg/kg) + diquat (API) group. We found that serum catalase (CAT) activity and total antioxidant capacity (T-AOC) markedly reduced in the RES and API groups as compared to the DIQ group (p < 0.05); moreover, serum S superoxide dismutase (SOD) levels increased significantly in the API group as compared to the DIQ group (p < 0.05). In jejunal mucosa, the malondialdehyde (MDA) content in the RES and API groups decreased more than that in the DIQ group (p < 0.05). In addition, the jejunal expression levels of the NRF2 and GCLM genes in the RES and API groups increased notably compared with those in the DIQ group (p < 0.05); meanwhile, CAT activity in the RES and API groups was markedly elevated compared with that in the CON group (p < 0.05). In IDECs, apigenin significantly restrained the H₂O₂-mediated increase in MDA content and decrease in CAT levels (p < 0.05). Furthermore, apigenin increased the protein expression of p-NRF2, NRF2, p-AKT, and p-P38; downregulated that of cleaved caspase-3 and cleaved caspase-9; and reduced the ratio of Bax/Bcl-2 in H₂O₂-treated IDECs (p < 0.05). In conclusion, resveratrol and apigenin can be used as natural feed additives to protect against jejunal oxidative stress in ducks.

Apigenin and sodium butyrate have been reported to help alleviate oxidative stress. This study evaluated the jejunal transcriptomic responses in ducks receiving apigenin and sodium butyrate supplementation under oxidative stress. In total, 200 healthy 300-day-old female Jinyun Ma ducks (1.53 kg ± 0.15) were randomly divided into four groups, with five replicates per group. The groups were as follows: a control group (CON): ducks were fed a basal diet with sterile saline injection; a diquat-injection (DIQ) group: ducks were fed a basal diet with diquat injection; an apigenin plus diquat group (API): ducks were fed a basal diet containing apigenin (500 mg/kg) with diquat injection; and a sodium butyrate plus diquat group (SB): ducks were fed a basal diet containing sodium butyrate (500 mg/kg) with diquat injection. The injection dose of diquat is 8 mg/kg body weight. Analysis revealed that the dietary supplementation of apigenin and sodium butyrate reduced malondialdehyde (MDA) levels and increased total antioxidant capacity (T-AOC) (p < 0.05). Compared to the DIQ group, sodium butyrate supplementation during oxidative stress elevated jejunal villus height and villus height/crypt depth ratio in ducks (p < 0.05). The study identified that some candidate genes, including solute carrier family 4 member 3 (SLC4A3), ADAM metallopeptidase domain 12 (ADAM12), and B-cell lymphoma 2-associated-athanogene 3 (BAG3), were significantly upregulated, whereas claudin 23 (CLDN23) and glucose-6-phosphatase catalytic subunit 1 (G6PC1) were markedly downregulated in the API group in comparison with that in the DIQ group (p < 0.05). Collectively, our findings provide molecular evidence for the beneficial effects of apigenin and sodium butyrate against oxidative stress in the jejunum of ducks.