Lauric acid (LA) has antimicrobial effects and the potential to replace antibiotics in feeds
to prevent postweaning diarrhea and increase overall swine productivity. The effects of lauric acid
on the intestinal epithelial cells remain unclear.
This study investigates the effects of LA on pig intestinal epithelial cell line (IPEC-J2) differentiation,
proliferation, and death and explores its underlying mechanisms. It was found that 0.25-0.1 mM LA
promoted IPEC-J2 cell differentiation. At 1 mM or higher concentrations, it induced IPEC-J2 cell
viability decreases, lipid accumulation, cell proliferation inhibition, and cell apoptosis. The cell death
induced did not depend on caspase pathways.
The data demonstrated that LA induced the IPEC-J2 cell autophagy and impaired autophagy flux
and autophagy plays a role in protecting against LA induced-cell death. p38 MAPK inhibitor
SB202190 attenuated LA-reduced IPEC-J2 cell viability. This associated with an increase in
autophagy level and a decrease in lipid accumulations and FABPI levels.
In summary, LA promoted the IPEC-J2 cell apoptosis depends on the p38 MAPK pathways and
may involve autophagy and TG metabolism regulation.