Submitted on January 21, 2009
Revised on May 21, 2009
Accepted on June 19, 2009
Role of Peroxisome Proliferators Activated Receptors 
(PPAR-) in ileum tight junction alteration in mouse model of restraint stress
Emanuela Mazzon1, Concetta Crisafulli, Maria Galuppo, and Salvatore Cuzzocrea1*
1 University of Messina
* To whom correspondence should be addressed. E-mail: salvator{at}unime.it.
Restraint stress induces permeability changes in the small intestine but little is known on the role of endogenous peroxisome proliferator-activated receptor-
(PPAR-) ligand in the defects of the TJ function. In the present study, we used PPAR- knock out mice (PPAR-KO) to understand the roles of endogenous PPAR- on ileum altered permeability function in models of immobilisation stress. The absence of a functional PPAR- gene in PPAR-KO mice resulted in a significant augmentation of the degree of (1) TNF- production in ileum tissues, (2) the alteration of Zonula occludens-1 (ZO-1), occludin and 
-catenin (immunohistochemistry) and (3) apoptosis (TUNEL staining, Bax, Bcl-2 expression). Taken together, our results demonstrate that endogenous PPAR- ligands reduce the degree of tight junction permeability in the ileum tissues associated with immobilisation stress, suggesting a possible role of endogenous PPAR- ligands on ileum barrier dysfunction.
