Temporal profile of intestinal tissue expression of intestinal fatty acid-binding protein in a rat model of necrotizing enterocolitis

Abstract

OBJECTIVES:Necrotizing enterocolitis is a severe multifactorial intestinal disorder that primarily affects preterm newborns, causing 20-40% mortality and morbidity. Intestinal fatty acid-binding protein has been reported to be a biomarker for the detection of intestinal injuries. Our aim was to assess intestinal tissue injury and the molecular expression of intestinal fatty acid-binding protein over time in a necrotizing enterocolitis model.METHODS:A total of 144 Newborn rats were divided into two groups: 1) Control, which received breastfeeding (n=72) and 2) Necrotizing Enterocolitis, which received formula feeding and underwent hypoxia and hypothermia (n=72). A total of six time points of ischemia (2 times a day for 3 days; 12 pups for each time point) were examined. Samples were collected for analysis of body weight, morphological and histological characteristics, intestinal weight, intestinal weight/body weight ratio, injury grade, and intestinal fatty acid-binding protein levels.RESULTS:Body and intestinal weights were lower in the Necrotizing Enterocolitis group than in the Control group (p<0.005 and p<0.0005, respectively). The intestinal weight/body weight ratio was higher in the Necrotizing Enterocolitis group than in the Control group (p<0.005) only at the sixth ischemia time point. The Necrotizing Enterocolitis group displayed higher expression of intestinal fatty acid-binding protein (p<0.0005) and showed greater tissue damage than the Control group.CONCLUSION:Intestinal fatty acid-binding protein was an efficient marker of ischemic injury to the intestine and a good correlation was demonstrated between the time of ischemic injury and the grade of intestinal injury.

Significance of dynamic evolution of TNF-α, IL-6 and intestinal fatty acid-binding protein levels in neonatal necrotizing enterocolitis

“…NEC is characterized by ischemic necrosis of gastrointestinal tract and intestinal perforation. The pathogenesis involves intestinal hypoxia-ischemia, immature intestinal development, microbial reproduction and high immune response of intestinal mucosa ( 13 , 14 ). I-FABP is mainly distributed in villus cells in intestinal mucosa, which can be quickly released when intestinal ischemic injury occurs, enters the blood circulation through the cell membranes, capillaries, lymphatic capillaries and portal veins, and is finally discharged with urine from the body ( 15 ).…”

The science and necessity of using animal models in the study of necrotizing enterocolitis

“…Rat NEC models have also been useful in temporal biomarker studies (e.g. correlation on intestinal fatty acid binding protein with timing of ischemia and severity of tissue injury(23)). Currently, the administration of a protein kinase A inhibitor(24) and milk-derived exosomes(25) are being studied in a rat model with promising results as potential treatments for NEC.…”

Crocodile Oil Disrupts Mitochondrial Homeostasis and Exacerbates Diabetic Kidney Injury in Spontaneously Diabetic Torii Rats

“…H&E staining was used to evaluate endothelial proliferation, mesangial proliferation, matrix accumulation, and interstitial inflammation, and PAS staining was examined for interstitial fibrosis. The severity of injury was graded (3 rats/group) by an experienced pathologist who was unaware of the treatment groups using a modified method previously described [ 25 , 26 ]. Arbitrary scores (au) were applied as follows: no change (0), no change or histopathological changes <10%; mild (0.5), 10–25%; moderate (1.0), 25–50%; and severe (1.5), >50%.…”