Abstract

To determine the expression of hepatic L-FABP and intestinal I-FABP in an experimental model of necrotizing enterocolitis (NEC) in neonatal rats. Newborn Sprague-Dawley rats were divided into four groups: Control (C1) - exclusive breastfeeding at the first and sixth procedures (C6), NEC1 - fed formula milk and submitted to hypoxia and hypothermia at the first and sixth procedures (NEC6). The newborn pups were fed twice a day for three days, for a total of six procedures. Samples were collected for morphometric evaluation (body weight, liver weight, liver weight/body weight ratio, intestinal weight and intestinal/body weight ratio) and for immunohistochemical and Western blotting analysis. The values obtained were analyzed statistically, with the level of significance set at p<0.05. Morphometric measurements showed reduction of body and liver weights in the NEC group (p<0.05). Both immunohistochemistry and western blotting revealed that L-FABP expression in the liver was decreased and I-FABP expression in the ileum was increased in the NEC group (p<0.05). L-FABP and I-FABP expression changed inversely in the rat NEC model. These findings can contribute to a better diagnosis of NEC in human newborns.

Highlights

  • MethodsNecrotizing enterocolitis (NEC) is a severe intestinal inflammatory disease affecting neonates, with a higher incidence among premature babies

  • Newborn Sprague-Dawley rats were divided into four groups: Control (C1) – exclusive breastfeeding at the first and sixth procedures (C6), NEC1 - fed formula milk and submitted to hypoxia and hypothermia at the first and sixth procedures (NEC6)

  • Samples were collected for morphometric evaluation and for immunohistochemical and Western blotting analysis

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Summary

Introduction

Necrotizing enterocolitis (NEC) is a severe intestinal inflammatory disease affecting neonates, with a higher incidence among premature babies. The disease is characterized by intestinal necrosis and leads to multiple organ failure[1]. The mortality rate associated with NEC ranges from 20 to 30%, with gastrointestinal sequelae such as stenosis and short bowel syndrome possibly being present in cases in which there is resolution or the need for surgical intervention[2]. Prematurity, bacterial infection, intestinal hypoxia-ischemia and enteral feeding are the major risk factors of the disease[3]. In severe cases of NEC, in addition to intestinal involvement there is a frequent occurrence of injury to one or more organs resulting in pulmonary, renal and/or hepatic failure[4]. Studies have reported significant pathological changes in hepatic morphology and in hepatobiliary function in patients with NEC, especially those submitted to parenteral nutrition[5]

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