Background:
Butyric acid (BT), a short-chain fatty acid, is the preferred
colonocyte energy source. The effects of BT on the differentiation, proliferation, and
apoptosis of small intestinal epithelial cells of piglets and its underlying mechanisms
have not been fully elucidated.
Methods:
In this study, it was found that 0.2-0.4 mM BT promoted the differentiation of
procine jejunal epithelial (IPEC-J2) cells. BT at 0.5 mM or higher concentrations
significantly impaired cell viability in a dose- and time-dependent manner. In addition, BT
at high concentrations inhibited the IPEC-J2 cell proliferation and induced cell cycle
arrest in the G2/M phase.
Results:
Our results demonstrated that BT triggered IPEC-J2 cell apoptosis via the
caspase8-caspase3 pathway accompanied by excess reactive oxygen species (ROS)
and TNF-α production. BT at high concentrations inhibited cell autophagy associated
with increased lysosome formation. It was found that BT-reduced IPEC-J2 cell viability
could be attenuated by p38 MAPK inhibitor SB202190. Moreover, SB202190 attenuated
BT-increased p38 MAPK target DDIT3 mRNA level and V-ATPase mRNA level that
were responsible for normal acidic lysosomes.
Conclusion:
In conclusion, 1) at 0.2-0.4 mM, BT promotes the differentiation of IPEC-J2
cells; 2) BT at 0.5 mM or higher concentrations induces cell apoptosis via the p38 MAPK
pathway; 3) BT inhibits cells autophagy and promotes lysosome formation at high
concentrations.
Sublytic C5b-9 Induces Glomerular Mesangial Cell Apoptosis through the Cascade Pathway of MEKK2–p38 MAPK–IRF-1–TRADD–Caspase 8 in Rat Thy-1 Nephritis