Abstract
Aim. Recombinant human trefoil factor 3 (intestinal trefoil factor) has been suggested to be partially protective against necrotizing enterocolitis (NEC), but the mechanisms of this protection have not been defined. We investigated whether the protective effects of rhTFF3 are the result of an anti-inflammatory response. Methods. The rats were killed on day 4, the distal ileum was harvested for morphological studies and immunohistochemistry for NF-κB (p65), and the amounts of IL-1β, IL-6, and IL-10 in the intestinal tissue were measured using commercial ELISA assay kits. Results. In the neonatal NEC, IL-1β, IL-6, and IL-10 were significantly higher than in normal group. In normal group, IL-1β and IL-6 were significantly decreased, and the amount of IL-10 was markedly increased compared with NEC group. In the NEC model, immunohistochemical staining for NF-κB (p65) was demonstrated to be of a strong brown color and was distributed in the intestinal epithelium. Treatment with rhTFF3 significantly decreased the immunoreactivity of NF-κB (p65) in the NEC model. Conclusions. Intestinal inflammation was ameliorated after rhTFF3 was injected. rhTFF3 may protect against the intestinal injury of the neonatal rat NEC model by suppression of the inflammatory response.
Highlights
For the past several years, due to the increasing survival rates of premature infants, the incidence and lethality of necrotizing enterocolitis (NEC) in neonates have increased
We previously demonstrated that rhTFF3 has a protective effect on intestinal injury in NEC in an experimental model [10], but the mechanisms of this protection are not yet defined
A positive control was established by giving rhTFF3 to detect NF-κB expression in enteral histopathological and immunohistological examinations, and the amounts of anti-inflammatory cytokines (IL-10) and proinflammatory cytokines (IL-6, IL-1β) following NEC were measured to determine whether the suppressed inflammatory response by rhTFF3 has a protective effect in the development of NEC
Summary
For the past several years, due to the increasing survival rates of premature infants, the incidence and lethality of necrotizing enterocolitis (NEC) in neonates have increased. Studies in recent years indicate that its pathogenesis is associated with premature delivery, intestinal ischemia-hypoxia damage, immature intestinal tract function, and the organism’s resistance, nutrition, and bacterial infection, among other factors [4] These risk factors are responsible for the production of inflammatory mediators and for activation of the local inflammation cascade; a series of changes occurs at the cellular level, and an overbalanced interaction between the intestinal necrosis proinflammatory cytokines and anti-inflammatory cytokines is triggered. The inflammatory cascade is started, leading to colon tissue immunologic injury, and a series of clinical symptoms appear Proinflammatory cytokines such as IL-1, IL-6, IL-8, and TNFα and anti-inflammatory cytokines such as IL-4, IL-10, and International Journal of Peptides. A positive control was established by giving rhTFF3 to detect NF-κB expression in enteral histopathological and immunohistological examinations, and the amounts of anti-inflammatory cytokines (IL-10) and proinflammatory cytokines (IL-6, IL-1β) following NEC were measured to determine whether the suppressed inflammatory response by rhTFF3 has a protective effect in the development of NEC
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