Restraint stress induces permeability changes in the small intestine, but little is known about the role of endogenous peroxisome proliferator-activated receptor-α (PPAR-α) ligand in the defects of the tight junction function. In the present study, we used PPAR-α knockout mice to understand the roles of endogenous PPAR-α on ileum altered permeability function in models of immobilization stress. The absence of a functional PPAR-α gene in PPAR-α knockout mice resulted in a significant augmentation of the degree of 1) TNF-α production in ileum tissues; 2) the alteration of zonula occludens-1, occludin, and β-catenin (immunohistochemistry); and 3) apoptosis (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining, Bax, Bcl-2 expression). Taken together, our results demonstrate that endogenous PPAR-α ligands reduce the degree of tight junction permeability in the ileum tissues associated with immobilization stress, suggesting a possible role of endogenous PPAR-α ligands on ileum barrier dysfunction.
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|Publication status||Published - Sep 2009|
- Peroxisome proliferator-activated receptor-α-deficient mice
- Zonula occludens-1
ASJC Scopus subject areas
- Physiology (medical)