Abstract
Background and Aims: This study was designed to investigate a relatively optimum dose of partial enteral nutrition (PEN) which effectively attenuates intestinal barrier dysfunction initiated by ischemia/reperfusion injury (IRI). Methods: In experiment 1, 60 male Sprague-Dawley (SD) rats were subjected to intestinal IRI and assigned to six groups according to the different proportion of EN administrations: namely total parenteral nutrition (TPN or 0%EN), 10%EN, 20%EN, 40%EN, 60%EN, and total enteral nutrition (TEN or 100%) groups, the deficits of intraluminal calorie were supplemented by PN. In experiment 2, 50 male SD rats were subjected to intestinal IRI and divided into five groups based on the results of experiment 1: TPN, TEN, 20%EN, TPN plus pretreatment with NF-κB antagonist 30 min before IRI (TPN+PDTC), and TPN plus pretreatment with HIF-1α antagonist 30 min before IRI (TPN+YC-1) groups. Results: In experiment 1, previous IRI combined with subsequent EN shortage disrupted the structure of intestinal epithelial cell and tight junctions (TJs). While 20% dose of EN had an obviously protective effect on these detrimental consequences. In experiment 2, compared with TPN only, 20%EN exerted a significant protection of barrier function of intestinal epithelium. Analogous results were observed when TPN combined with specific NF-κB/HIF-1α inhibitors (PDTC and YC-1). Meanwhile, the expression of NF-κB/HIF-1α had a similar trend among the groups. Conclusions: Our findings indicate that 20%EN is the minimally effective dosage of EN which promotes the recovery of intestinal barrier function after IRI in a rat model. Furthermore, we discreetly speculate that this benefit is, at least partly, related to NF-κB/HIF-1α pathway expression.
Highlights
Ischemia reperfusion injury (IRI) is a pathophysiologic process in which hypoxic organ damage is deteriorated following restoration of blood flow and oxygen delivery to the ischemic tissue [1,2,3].The intestinal mucosal epithelium is susceptible to decreased mesenteric blood flow after the interruption of oxygen and nutrients [4]
After 6-day treatment, phosphorylated nuclear factor (NF)-κB proteins (p65) were significantly increased in the total parenteral nutrition (TPN) and 10%enteral nutrition (EN) groups compared with other groups (Figure 1A,B)
hypoxia-inducible factor (HIF)-1β showed no difference between all the groups as expected (Figure 1C). 20%EN and 40%EN rats significantly reduced in expression (p < 0.05) and in 60%EN and TEN rats, this difference (p < 0.01) was more significant
Summary
Ischemia reperfusion injury (IRI) is a pathophysiologic process in which hypoxic organ damage is deteriorated following restoration of blood flow and oxygen delivery to the ischemic tissue [1,2,3]. A study of a dextran sulfate sodium-induced colitis model confirmed that knockout of HIF-1α in dendritic cells led to more severe intestinal inflammation, increased levels of proinflammatory cytokines, and enhanced production of mucin [13]. These results indicated that HIF-1α may have a potentially protective effect in inflammation of intestinal tissue. Because PN without enteral feeding is associated with a greater risk of infection and impaired gut-derived immune responses, we hypothesized that the deficiency of enteral feeding activates the NF-κB/HIF-1α signaling pathway despite complete reperfusion, leading to impairment of the intestinal mucosa barrier. We hypothesized that PEN inhibits expression of the NF-κB/HIF-1α signaling pathway in a rat model of intestinal IRI
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