Roles Of Neutrophil Extracellular Traps In Intestinal Ischemia-Reperfusion Injury

Objective: we aimed to determine whether neutrophil extracellular traps(NETs) involved in intestinal ischemia-reperfusion injury of intestinal mucosa injury and aggravated, and whether it is possible to improve the degree of intestinal mucosal injury by depredating the Nets.Methods : 54 wistar rats with half males and half females were randomly assigned into control group(n=6), ischemia-reperfusion group(n=24) and ischemia-reperfusion+ DNase-1 injection group(n=24). The latter two groups were divided into 4 subgroups respectively according to the length of reperfusion(2h, 6h, 12 h, and 24h). Ischemia-reperfusion was performed by ligation of the superior mesenteric artery and released it in 1h. Intravenously, DNase-1 at 10mg/KG was injected 15 min before the release. The blood and the small intestine were taken for further investigation after sacrificing. Animals in the sham-control group had their superior mesenteric artery exposed but not ligated. The blood and the small intestines were taken 2h post the manipulation. The expression of citrullinated histones H3, super oxidase dismutase, malonaldehyde, TNF-α and endotoxin in plasma or intestinal tissue were investigated by ELISA. Pathological examination was performed according to Chiu`s rating criteria to assess the injury of intestinal mucosa.Results: 1.Plasma cit H3 level in group B was significantly higher than that in group A except the B-24 h subgroup. This difference was also demonstrated in the small intestine. Plasma TNF-α level in group B was significantly higher than that in group A. The same difference was observed in the intestinal tissue. Compared with control group, plasma endotoxin level in group B was much higher. The plasma SOD level in group B was lower than that in group A with B-12 h the minimal. The difference was confirmed in the intestinal tissue. The plasma MDA level in group B was high than that in group A and the subgropup B-12 h was the maximum. This difference was also demonstrated in the small intestine. Compared with control group, intestinal mucosa Injury score in group B was much higher with B-12 h the highest. 2. Plasma cit H3 level in group C was significantly lower than that in group B except the c-6, c-24 subgroups. Intestinal cit H3 expression in group C was significantly lower than that in group B except the c-12, c-24 subgroups. Plasma TNF-α level in group C except c-24 was significantly lower than that in group B. Intestinal TNF-α level in group C was significantly lower than that in group B. Except for the C-6h subgroup, plasma endotoxin level in group C was lower than that in group B and it decreased as reperfusion time increased. The plasma SOD level in group C except the subgroup C-12 h was higher than that in group B. The intestinal SOD expression in group C was higher than that in group B. The plasma MDA level in group C except the subgroup C-6h was lower than that in group B. The intestinal MDA level in group C was lower than that in group B. The score in group C except C-2h and C-6h was significantly lower than that in group B.Conclusion : 1. Cit H3 significantly increased during intestinal ischemiareperfusion injury in rat plasma and intestinal tissue. 2. After 12 h of intestinal ischemia-reperfusion in rat, the most serious peroxidation damages were presented and the intestinal mucosa is also seriously injured. 3. Degrading NETs can reduce peroxidation damages and the injury of intestinal mucosa after intestinal ischemia-reperfusion injury.