Title:The Effects of Lauric Acid on IPEC-J2 Cell Differentiation, Proliferation, and Death
Volume: 20
Issue: 7
Author(s): Yuan Yang, Jin Huang, Jianzhong Li, Huansheng Yang*Yulong Yin
Affiliation:
- Hunan International Joint Laboratory of Animal Intestinal Ecology and Health, Nutrition and Human Health Laboratory, School of Life Sciences, Hunan Normal University, Changsha City, Hunan 410081,China
Keywords:
lauric acid, IPEC-J2 cell, p38 MAPK, triglyceride, FABPI, autophagy.
Abstract:
Background: 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.
Methods and Results: 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.
Conclusion: In summary, LA promoted the IPEC-J2 cell apoptosis depends on the p38 MAPK
pathways and may involve autophagy and TG metabolism regulation.
