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

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 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].

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.