RESUMO
Necrotizing enterocolitis (NEC), a serious gastrointestinal inflammatory disease, frequently occurs in preterm neonates that fail to adapt to enteral nutrition. A temporal gel-based proteomics study was performed on porcine intestine with NEC lesions induced by enteral formula feeding. Functional assignment of the differentially expressed proteins revealed that important cellular functions, such as the heat shock response, protein processing; and purine, nitrogen, energy metabolism, were possible involved in the early progression of NEC.
Assuntos
Nutrição Enteral/efeitos adversos , Enterocolite Necrosante/diagnóstico , Enterocolite Necrosante/metabolismo , Mucosa Intestinal/metabolismo , Apoio Nutricional/efeitos adversos , Proteômica/métodos , Animais , Animais Recém-Nascidos , Modelos Animais de Doenças , Eletroforese em Gel Bidimensional , Enterocolite Necrosante/veterinária , Perfilação da Expressão Gênica/métodos , Processamento de Imagem Assistida por Computador , Intestinos/patologia , Espectrometria de Massas/métodos , Nascimento Prematuro , Suínos , Fatores de TempoRESUMO
Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in newborn premature infants. Clinical studies show increased incidence of NEC in premature infants with enteral formula feeding; however, pathogenesis remains unclear. To identify the NEC-related proteins for molecular mechanisms, we applied proteomics analysis to characterize changes in the protein expression profile of newborn premature piglet intestines with NEC developed after enteral formula feeding for 24 h. Changes in protein expression were identified using 2-dimensional gel electrophoresis and peptide mass fingerprinting with MS as well as western blotting analysis. Nineteen differentially expressed proteins were identified and these have roles in oxidative stress, chaperone, signal transduction, protein folding and degradation, oxygen transport, signal transduction, and energy metabolism. Proteins with increased levels include manganese-containing superoxide dismutase and hemoglobin subunit and proteins with decreased expression include sorbitol dehydrogenase, mitochondrial aldehyde dehydrogenase 2, glucose-regulated protein 75, CRY protein, snail homolog 3, thyroid hormone-binding protein precursor, and DJ1 (Parkinson's disease 7) etc. The data provided novel mechanistic insights into the pathogenesis of NEC and the insults of a formulated diet to the premature gut.
