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
Summary
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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