Intestinal tract and parenteral multi-organ sequential pathological injury caused by necrotizing enterocolitis

Abstract

Background: To explore the relationship between the pathological changes of the colon, terminal ileum, lung, liver and kidney, and the changes of Bax, PCNA and PAF in a rat model of NEC. Methods: 140 neonatal SD rats were randomly divided into NEC group and control group (70 in each group). NEC group was given hypoxia, cold stimulation and artificial feeding twice a day for 3 consecutive days. The control group was only fed normally. After modeling, From the 1st day to the 7th day, 10 rats were sampled in each group for pathological examination of colon, terminal ileum, lung, liver and kidney tissue. The levels of Bax, PCNA and PAF were investigated by immunohistochemistry. Results: Compared with the normal group, in the NEC group, on the 1st day, the colon, terminal ileum, lung, liver and kidney showed inflammatory damage. On the 5th day, the inflammatory injury was reduced. The inflammation disappeared on the 7th day. There were differences in the time of apoptosis in the intestine. In the intestine, the proliferation of PCNA was weak at first and then strong. Bax in liver and kidney showed marked apoptosis and apoptosis time increased in the lung. The expression of PCNA increased in lung, liver and kidney, and the expression of PAF increased in lung and liver. Conclusions: NEC can lead to secondary injury of different degrees in colon, terminal ileum, lung, liver and kidney, and the degree and time of injury and repair were different. In general, organ repair played a leading role on the 4th day after modeling.

Comparison and Investigation of Exosomes from Human Amniotic Fluid Stem Cells and Human Breast Milk in Alleviating Neonatal Necrotizing Enterocolitis

“…However, current studies have been limited to the therapeutic effects on NEC-associated intestinal injury and inflammation. NEC is not only an intestinal disease [25,26], but its broader sequelae include systemic inflammation, hypoxia, ischemia, and multi-system organ dysfunction in severe cases, particularly affecting brain function [27]. The alleviating effect of AFSC-exos and HBM-exos on systemic inflammation in our study has been mentioned previously.…”

The administration of a pre-digested fat-enriched formula prevents necrotising enterocolitis-induced lung injury in mice

“…The current study focuses on strategies to prevent the development of NEC-induced lung injury, which remains a major cause of morbidity and mortality in patients with NEC, and for which there are few effective treatment strategies (37) . Prior investigators have shown that the development of lung injury in NEC involves a coordinated proinflammatory response within the lung parenchyma that results in impaired healing within the pulmonary epithelium (38) . We have previously shown that NEC-induced lung injury results in part from activation of the bacterial receptor toll-like receptor 4 (TLR4) on the pulmonary epithelium which results in an influx of inflammatory neutrophils and a destruction of the alveolar membrane (14) .…”