Abstract
Objective: MicroRNA-141-3p (miR-141-3p) has been investigated in various kinds of cancers. This research delves into the functions and regulatory mechanisms of miR-141-3p in necrotizing enterocolitis (NEC) of neonates.Methods: NEC tissues were obtained from neonatal mice, and subsequently, expression of miR-141-3p and motor neuron and pancreas homeobox 1 (MNX1) was assayed via RT-qPCR. Moreover, the intestinal histopathological changes and histiocytic apoptosis were observed via hematoxylin and eosin (H&E) and TUNEL staining. The correlative inflammatory factors and oxidative stress markers were evaluated to uncover the influence of miR-141-3p in NEC tissue damage. Further, the relation between MNX1 and miR-141-3p was predicated, and the functions of MNX1 in inflammatory response and cell growth of IEC-6 cells were investigated.Results: Downregulated miR-141-3p and upregulated MNX1 were discovered in NEC tissues. Moreover, miR-141-3p clearly alleviated inflammation response and oxidative stress damage in NEC, which was achieved through regulating inflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative stress markers (MPO, MDA, and SOD) expression. MNX1 was forecasted as a target gene of miR-141-3p; meanwhile, MNX1 overexpression overturned the influence of miR-141-3p in the inflammatory response and cell growth process of IEC-6 cells.Conclusion: These explorations reveal that increased expression of miR-141-3p could improve the damage to intestinal tissues in NEC through targeting MNX1. The research might exhibit a neoteric therapeutic strategy for NEC.
Highlights
Necrotizing enterocolitis (NEC) is an acquired illness, which is the most familiar neonatal gastrointestinal emergency, and it is a dominating reason for intestinal perforation and systemic inflammatory response syndrome (SIRS) in neonates [1, 2]
The NEC tissues obtained from eight male C57BL/6 neonatal mice were used in the experiment; thereafter, the RT-qPCR assay was carried out to examine miR-141-3p and Motor neuron and pancreas homeobox 1 (MNX1) expression in NEC tissues
These consequences revealed the aberrant expression of miR141-3p and MNX1 in NEC tissues
Summary
Necrotizing enterocolitis (NEC) is an acquired illness, which is the most familiar neonatal gastrointestinal emergency, and it is a dominating reason for intestinal perforation and systemic inflammatory response syndrome (SIRS) in neonates [1, 2]. NEC affects digestive system function, and severe cases can cause systemic symptoms, such as shock, acidosis, and jaundice [3, 4]. The representative symptoms of NEC in the clinic incorporate abdominal distension, vomiting, Functions of miR-141-3p in NEC diarrhea, and bloody stools [5]. There are advances in neonatal nursing, NEC is still a leading cause of morbidity and mortality in premature infants [7]. To clarify the pathogenesis of NEC and explore its possible diagnostic and therapeutic targets will be beneficial to the clinical therapy of this disease
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