Eckol alleviates intestinal dysfunction during suckling-to-weaning transition via modulation of PDX1 and HBEGF

Background Maintaining intestinal health in livestock is critical during weaning. Although intestinal dysfunction during this period can be alleviated by phlorotannins including eckol, the precise mechanisms are not fully understood. We addressed this question by evaluating changes in gene expression and intestinal function after treatment with eckol during the suckling-to-weaning transition. The biological roles of differentially expressed genes in intestinal development were investigated by assessing intestinal wound healing and barrier function and associated signaling pathways, along with oxidative stress levels. Results We identified 890 differentially expressed genes in the intestine whose expression was altered by eckol treatment including pancreatic and duodenal homeobox (PDX)1, which directly regulate the expression of heparin-binding epidermal growth factor-like growth factor (HBEGF) to preserve intestinal barrier function and promote wound healing via phosphoinositide 3-kinase (PI3K)/AKT and P38 signaling. Additionally, eckol alleviated H2O2-induced oxidative stress via PI3K/AKT, P38, and 5' AMP-activated protein kinase signaling, improved growth, and reduced oxidative stress and intestinal permeability in pigs during weaning. Conclusions Eckol modulates intestinal barrier function, wound healing, and oxidative stress via PDX/HBEGF and improves growth during the suckling-to-weaning transition, suggesting that it can be used as a feed supplement to preserve intestinal function during this process in pigs and other livestock.