Pathological changes of colonic, ileal, lung, liver and kidney injury induced by NEC
On the 1st day after the establishment of the NEC model, we observed intestinal villi falling off, structure disappearance caused by necrosis, submucosal and muscular edema, intestinal wall congestion, hemorrhage, and necrosis accompanied by infiltration by many inflammatory cells, mainly neutrophils. Histological scores centered at 3 and 4 points on Day 1, but decreased to 2 points by the 3rd to 5th day, and became <1 on the 7th day.
In the observation group, on the first day after modeling, pulmonary epithelium, pulmonary interstitial and renal interstitial edema was accompanied with inflammatory cell infiltration, and inflammatory exudates were seen in the alveolar cavities and bronchi, vacuolar degeneration of hepatocytes, infiltration of inflammatory cells around necrotic foci, ischemic changes of glomeruli and obvious edema of the proximal convoluted tubule cells. On the third day, alveolar walls continued to thicken, interstitial edema was obvious, vacuolar degeneration of the liver was alleviated, necrosis of the liver was reduced, the cytoplasm was still loose, glomerular congestion was obvious, and tubular cells were still edematous. On the fifth day, pulmonary edema and interstitial thickening were significantly alleviated, and by the 7th day, alveolar inflammatory exudation and absorption were more obvious, hepatic inflammatory cell infiltration was reduced, and glomerular congestion and tubular edema were significantly alleviated.
Bax expression in colonic, ileal, lung, liver and kidney
Bax was expressed in intestinal villi epithelial cells, bronchial epithelial cells, inflammatory cells in the pulmonary interstitium and the alveolar area, hepatocytes, renal corpuscles, tubules and medulla. The expression of Bax in the intestinal tract of the NEC group was stronger than that in the control group. Bax expression gradually decreased with time and reached a minimum on the 7th day. The expression of Bax in lung, liver and kidney in the observation group was higher than that in the control group (P<0.05). Among them, the expression of Bax in the lung of the observation group showed a gradually increasing trend to a higher level up to the 5th day after modeling, and then gradually decreased on the 1st day, and then stabilized after the 5th day. In the kidney, decreased gradually from the first day to the third day, then tended to be stable (Figure 1).
PCNA expression in colonic, ileal, lung, liver and kidney
PCNA is expressed in intestinal epithelial cells, lung epithelium, hepatocytes, interstitial lung, renal cortex and tubular nucleus of the renal corpuscle. In the NEC group, the expression of PCNA on the 1st day after modeling was lower than that of control group. Expression gradually increased to the 4th and 5th day. Quantitative analysis showed that the expression of PCNA in lung, liver and kidney in the observation group was higher than that in the control group (P<0.05), except for the lower expression of PCNA in liver on Day 1. The expression of PCNA in the lungs of the observation group was higher than that of the normal control group on the 1st day after modeling, and gradually increased to the 3rd day and then decreased to the 7th day. The expression in liver gradually increased up to Day 3 and remained stable. The expression increased gradually in the kidney (Figure 2).
PAF expression in colonic, ileal, lung, liver and kidney
The expression of PAF was the same as that of Bax. In the NEC group, expression of PAF was higher than that of control group on the 1st day, then increased gradually up to the 4th day, after which expression began to decrease and approached normal levels by the 7th day. In the observation group, the expression of PAF gradually increased to the maximum at the 4th day after lung modeling, and then gradually decreased. In the liver, it increased gradually from the 2nd day to the 4th day, and then decreased gradually. However, 1-7 days after termination of NEC induction, its expression in the kidney was stable. Quantitative analysis showed that the expression of PAF in the lung and liver of the observation group was higher than that of the control group (P< 0.05), but there was no significant difference in the expression of PAF in the kidney (P> 0.05) (Figure 3).