Comparison of Necrotizing Enterocolitis-related apoptosis factors in the ileum of lipopolysaccharide and hypoxia-treated full-term and pre-term rats

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Abstract The aim of this study was to determine whether endotoxin, hypoxia, and prematurity are risk factors for developing necrotizing enterocolitis (NEC), which was achieved by investigating the pathogenesis of necrotizing enterocolitis in rats. To this end, we used premature Sprague-Dawley (SD) rat pups delivered by cesarean section at a gestational age of 21 days (Pre-term group) as well as Full-term SD rat pups four days after birth (Full-term group). The pups were exposed to lipopolysaccharides (LPS) and hypoxia to induce necrotizing enterocolitis. It was seen that both Full- and Pre-term rats were resulted in necrotizing enterocolitis. The results indicated that, compared to the control groups, the degree of apoptosis was elevated in both the Pre-term and Full-term NEC rats. The Full-term group also showed a reduction in Bcl-2 levels and an elevation in the ratio of Bax-to-Bcl-2 levels compared to the control group. Meanwhile, the Pre-term group showed a significantly increased expression level of RIPK1, which implies the induction of RIPK1-dependent apoptosis. This suggests that the pathophysiology of necrotizing enterocolitis induced by LPS+ hypoxia is associated with programmed cell death pathway. It appears that the apoptotic pathway of the Bax/Bcl-2 system is the main mechanism in Full-term rats. By contrast, a number of other mechanisms, including TNF-induced apoptosis mechanism, may work together for necrotizing enterocolitis development in Pre-term rats. Further studies are needed to elucidate the different pathogenesis of necrotizing enterocolitis development between Pre-term and Full-term rats.

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