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. 2003 Jan;36(1):126-33.
doi: 10.1097/00005176-200301000-00024.

Ileal cytokine dysregulation in experimental necrotizing enterocolitis is reduced by epidermal growth factor (V体育安卓版)

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Ileal cytokine dysregulation in experimental necrotizing enterocolitis is reduced by epidermal growth factor (V体育2025版)

Melissa D Halpern et al. J Pediatr Gastroenterol Nutr. 2003 Jan.

Abstract

Background: Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants VSports手机版. We have shown in previous studies that proinflammatory interleukin-18 and interleukin-12 are up-regulated in the ileum of rats with experimental NEC and that epidermal growth factor (EGF) reduces the development of disease. Here we investigated whether the protective effects of EGF are a result of changes in ileal interleukin-18, interleukin-12 and/or antiinflammatory interleukin-10. .

Methods: Newborn rats were artificially fed with either growth-factor-free rat milk substitute (RMS) or RMS supplemented with 500 ng/mL EGF (RMS + EGF) and NEC was induced via exposure to asphyxia and cold stress V体育安卓版. Cytokine expression and localization were assessed using reverse-transcription real-time polymerase chain reaction and immunohistology/confocal microscopy. .

Results: Enteral administration of EGF (RMS + EGF) decreased overproduction of interleukin-18 and increased interleukin-10 production in the ileum. Furthermore, increased interleukin-10 production was associated with up-regulation of the transcription factor Sp1 in RMS + EGF rats V体育ios版. .

Conclusions: These data suggest that EGF may reduce NEC via increased interleukin-10 and decreased interleukin-18 and that EGF-mediated up-regulation of Sp1 may account for the increased interleukin-10. VSports最新版本.

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