自噬
程序性细胞死亡
细胞凋亡
月桂酸
细胞生物学
活力测定
细胞生长
p38丝裂原活化蛋白激酶
细胞
生物
化学
MAPK/ERK通路
信号转导
生物化学
脂肪酸
作者
Yuan Yang,Huang Jin,Jianzhong Li,Huansheng Yang,Yulong Yin
标识
DOI:10.2174/1566524020666200128155115
摘要
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.
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