The effect of vascular endothelial growth factor overexpression in experimental necrotizing enterocolitis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-03

AUTHORS

Hande Ozgun Karatepe, Huseyin Kilincaslan, Mustafa Berber, Ahmet Ozen, Hulya Ercan Saricoban, Duran Ustek, Ahu Sarbay Kemik, Mine Adas, Filiz Bakar

ABSTRACT

PURPOSE: 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. MATERIALS AND METHODS: 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 μg) incorporated into plasmid (2 μg) 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]. RESULTS: 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). CONCLUSION: VEGF overexpression with plasmids seems to be a promising approach in the management of NEC. More... »

PAGES

327-332

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00383-013-3460-z

DOI

http://dx.doi.org/10.1007/s00383-013-3460-z

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050421582

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24380924


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48 schema:description PURPOSE: 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. MATERIALS AND METHODS: 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 μg) incorporated into plasmid (2 μg) 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]. RESULTS: 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). CONCLUSION: VEGF overexpression with plasmids seems to be a promising approach in the management of NEC.
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