The effect of vascular endothelial growth factor overexpression in experimental necrotizing enterocolitis
The effect of vascular endothelial growth factor overexpression in experimental necrotizing enterocolitis
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DOI：
10.1007/s00383-013-3460-z
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发表时间：
2014-03-01
影响因子：
1.8
通讯作者：
Bakar, Filiz
中科院分区：
文献类型：
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作者：
Karatepe, Hande Ozgun;Kilincaslan, Huseyin;Bakar, Filiz
坏死性小肠结肠炎（NEC）是一种严重疾病，主要见于早产儿。为探讨血管内皮生长因子（VEGF）对NEC的影响，将24只新生Wistar白化病大鼠随机分为对照组、NEC组和NEC+VEGF组。NEC由高渗性肠内配方喂养、暴露于缺氧/复氧和冷应激诱导。在NEC+VEGF组中，从NEC程序的第一天开始，每天一次皮下施用掺入质粒（2 μ g）中的VEGF（1 μ g），总共3天。所有大鼠在出生后第4天处死，收集标本进行组织病理学和生化检查[包括组织氧化应激（丙二醛和一氧化氮），炎症（髓过氧化物酶、白细胞介素-6和肿瘤坏死因子α）与细胞凋亡在NEC+VEGF组中，组织丙二醛、一氧化氮、白细胞介素-6，肿瘤坏死因子α水平和半胱天冬酶-3活性显著降低。此外，髓过氧化物酶水平与NEC组相比升高（p < 0.05）。组织学检查显示VEGF过表达可促进新生血管生成，减轻绒毛萎缩和组织水肿（p < 0.05），VEGF质粒过表达有望成为治疗NEC的有效方法。
Necrotizing enterocolitis (NEC) is a serious condition, predominantly observed in premature infants. We used an experimental NEC model to investigate the effects of vascular endothelial growth factor (VEGF) cloned into a plasmid.Twenty-four newborn Wistar albino rats were randomized equally into three groups as follows: control, NEC and NEC+VEGF. NEC was induced by hyperosmolar enteral formula feeding, exposure to hypoxia/reoxygenation and cold stress. In the NEC+VEGF group, VEGF (1 mu g) incorporated into plasmid (2 mu g) was administered subcutaneously once daily for a total of 3 days starting on the first day of the NEC procedure. All rats were sacrificed on the 4th day of life, and the specimens were harvested for histopathological and biochemical examinations [including tissue oxidative stress (malondialdehyde and nitric oxide), inflammation (myeloperoxidase, interleukin-6 and tumor necrosis factor alpha) and apoptosis (caspase-3 activity) parameters].In the NEC+VEGF group, tissue malondialdehyde, nitric oxide, interleukin-6, tumor necrosis factor alpha levels and caspase-3 activity were significantly decreased. In addition, the myeloperoxidase level was increased compared to that of the NEC group (p < 0.05). Histopathologically, VEGF overexpression enhanced angiogenesis, alleviated villous atrophy and tissue edema (p < 0.05).VEGF overexpression with plasmids seems to be a promising approach in the management of NEC.