BACKGROUND & AIMS: This study was designed to investigate whether n-3 PUFAs attenuate ischemia/reperfusion (I/R) induced intestinal barrier injury by activating I-FABP-PPARγ pathway. METHODS: 24 Male Sprague-Dawley rats were assigned to 4 groups: control group, I/R group, pretreated with n-3 PUFAs for 7 days before I/R (group 3), pretreated with peroxisome proliferator-activated receptor (PPARγ) agonist 30 min before I/R (group 4). The serum and intestinal mucosa samples were collected. RESULTS: I/R disrupted the structure of intestinal tight junctions (TJs) and reduced occludin expression. The intestinal fatty acid binding protein (I-FABP) was elevated in plasma while decreased in cells. PPARγ expression in nucleus of intestinal mucosa was attenuated. N-3 PUFAs attenuated the damaged TJ structure and elevated occludin, intracellular I-FABP and PPARγ expression. A PPARγ agonist had the same effect as n-3 PUFAs. CONCLUSIONS: The intestinal barrier is severely damaged after I/R, which is related to the redistribution of I-FABP. Our findings firstly indicate that n-3 PUFAs protect the intestinal barrier by modifying intracellular I-FABP, activating the PPARγ pathway, and then upregulating TJ protein expression.
BACKGROUND & AIMS: This study was designed to investigate whether n-3 PUFAs attenuate ischemia/reperfusion (I/R) induced intestinal barrier injury by activating I-FABP-PPARγ pathway. METHODS: 24 Male Sprague-Dawley rats were assigned to 4 groups: control group, I/R group, pretreated with n-3 PUFAs for 7 days before I/R (group 3), pretreated with peroxisome proliferator-activated receptor (PPARγ) agonist 30 min before I/R (group 4). The serum and intestinal mucosa samples were collected. RESULTS: I/R disrupted the structure of intestinal tight junctions (TJs) and reduced occludin expression. The intestinal fatty acid binding protein (I-FABP) was elevated in plasma while decreased in cells. PPARγ expression in nucleus of intestinal mucosa was attenuated. N-3 PUFAs attenuated the damaged TJ structure and elevated occludin, intracellular I-FABP and PPARγ expression. A PPARγ agonist had the same effect as n-3 PUFAs. CONCLUSIONS: The intestinal barrier is severely damaged after I/R, which is related to the redistribution of I-FABP. Our findings firstly indicate that n-3 PUFAs protect the intestinal barrier by modifying intracellular I-FABP, activating the PPARγ pathway, and then upregulating TJ protein expression.