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首页> 外文期刊>American Journal of Physiology >Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis.
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Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis.

机译：表皮生长因子在坏死性小肠结肠炎的实验模型中减少肠道凋亡。

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摘要

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Although end-stage NEC is characterized histopathologically as extensive necrosis, apoptosis may account for the initial loss of epithelium before full development of disease. We have previously shown that epidermal growth factor (EGF) reduces the incidence of NEC in a rat model. Although EGF has been shown to protect intestinal enterocytes from apoptosis, the mechanism of EGF-mediated protection against NEC is not known. The aim of this study was to investigate if EGF treatment elicits changes in expression of apoptotic markers in the ileum during the development of NEC. With the use of a well-established neonatal rat model of NEC, rats were divided into the following three experimental groups: dam fed (DF), milk formula fed (NEC), or fed with formula supplemented with 500 ng/ml EGF (NEC+EGF). Changes in ileal morphology, gene and protein expression, and histological localization of apoptotic regulators were evaluated. Anti-apoptotic Bcl-2 mRNA levels were markedly reduced and pro-apoptotic Bax mRNA levels were markedly elevated in the NEC group compared with DF controls. Supplementation of EGF into formula significantly increased anti-apoptotic Bcl-2 mRNA, whereas pro-apoptotic Bax was significantly decreased. The Bax-to-Bcl-2 ratio for mRNA and protein was markedly decreased in NEC+EGF animals compared with the NEC group. The presence of caspase-3-positive epithelial cells was markedly reduced in EGF-treated rats. These data suggest that alteration of the balance between pro-and anti-apoptotic proteins in the site of injury is a possible mechanism by which EGF maintains intestinal integrity and protects intestinal epithelium against NEC injury.
机译：坏死性小肠结肠炎（NEC）是一种破坏性的早产儿肠道疾病。尽管终末NEC在组织病理学上被表征为广泛的坏死，但凋亡可能是疾病完全发展之前上皮细胞最初的丧失的原因。先前我们已经表明，表皮生长因子（EGF）可以降低大鼠模型中NEC的发生率。尽管已显示出EGF保护肠肠细胞免于细胞凋亡，但EGF介导的针对NEC的保护机制尚不清楚。这项研究的目的是调查EGF治疗在NEC发生过程中是否引起回肠细胞凋亡标记物表达的变化。使用成熟的NEC新生大鼠模型，将大鼠分为以下三个实验组：大坝喂养（DF），牛奶配方喂养（NEC）或补充有500 ng / ml EGF的配方喂养（NEC + EGF）。评估回肠形态，基因和蛋白质表达的变化，以及凋亡调节因子的组织学定位。与DF对照相比，NEC组的抗凋亡Bcl-2 mRNA水平显着降低，促凋亡Bax mRNA水平显着升高。向配方中添加EGF可以显着提高抗凋亡Bcl-2 mRNA的表达，而促凋亡Bax则显着降低。与NEC组相比，NEC + EGF动物中mRNA和蛋白质的Bax / Bcl-2比明显降低。经EGF处理的大鼠中caspase-3阳性上皮细胞的存在明显减少。这些数据表明，损伤部位的促凋亡蛋白和抗凋亡蛋白之间的平衡改变是EGF维持肠道完整性并保护肠上皮免受NEC损伤的可能机制。

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