Integration analysis of transcriptomics and proteomics reveals molecular pathways of duck intestinal epithelial cells...

Previous studies have shown that ducks undergo stress when transferred to a cage, and intestinal oxidative damage is induced. The intestinal mucosa is an important target of stress, and the terminal intestinal epithelial cells of the villi are the most strongly affected by oxidative stress. To investigate the molecular mechanism of oxidative damage in duck intestinal epithelial cells (dIECs), damage to dIECs was detected by inducing oxidative stress with different concentrations (0, 50, 100, and 200 μM) of hydrogen peroxide (H₂O₂) in primary dIECs, and molecular pathways were analyzed using combined transcriptomics and proteomics. The results revealed that oxidative stress significantly increased the reactive oxygen species (ROS) levels and apoptosis rate (P < 0.05), decreased antioxidant activity and intestinal barrier-related gene expression (P < 0.05), and caused nuclear irregularity, mitochondrial damage and vacuolization. A total of 766 differentially expressed genes (DEGs) and 566 differentially expressed proteins (DEPs) were screened by transcriptome and proteome sequencing. GO and KEGG enrichment analyses revealed that the DEGs and DEPs were enriched in pathways such as the T-cell receptor signaling pathway, apoptosis signaling pathway, cellular response to tumor necrosis factor, glycolysis/gluconeogenesis, steroid hormone biosynthesis, retinol metabolism, PPAR signaling pathway, FoxO signaling pathway, arachidonic acid metabolism, retinol metabolism, and cytochrome P450 metabolic pathway. In addition, key genes at the intersection of multiple pathways, such as PCK1 and HPGDS, were identified. In conclusion, H₂O₂-induced oxidative stress resulted in oxidative damage and increased the permeability of dIECs, leading to apoptosis and intestinal barrier damage. Multiomics analyses revealed that cellular homeostasis, immune response and metabolic regulation signaling pathways are important molecular pathways involved in the response of dIECs to oxidative stress. These findings elucidate the molecular biological process of duck intestinal epithelial injury and provide a molecular theoretical basis for research to improve duck intestinal health.