IL-1β诱导NF-κB通路对肠三叶因子治疗坏死性小肠结肠炎的影响及意义

Experiment on intestinal trefoil factor by IL-1β-induced NF-κB in the treatment for necrotizing enterocolitis in mice

目的研究肠三叶因子（ITF）对坏死性小肠结肠炎（NEC）新生大鼠的肠黏膜中自细胞介素1β（IL-1β）含量的影响，观察ITF对NEC新生大鼠中核因子-κB（NF-κB）的活化及胞内分布规律，探讨其在NEC发病机制中的作用。方法50只新生Wistar大鼠随机分为5组（正常对照组、正常对照给予ITF组、NEC模型组、NEC给予生理盐水组、NEC给予ITF组），每组10只，并于NEC模型后，母鼠身边喂养3d。第四天处死并取回盲部组织1～2cm固定、包埋、切片、HE染色，观察组织学变化及免疫组化表现NF-κB的表达，其他肠组织制备组织匀浆，取上清液检测IL-1β含量。结果NEC新生大鼠模型中损伤肠组织IL-1β含量明显增多，NF-κB表达增强。ITF治疗组能明显的抑制NEC新生大鼠肠组织IL-1β的产生和NF-κB（P65）的表达。结论NF-κB信号通路可能参与了NEC发病过程，并起着信号转导作用；ITF通过抑制NF-κB信号通路，减轻小肠结肠组织炎症反应，起到保护肠黏膜的作用。

Objective To study the effects of intestinal trefoil factor （ITF） on the interleukin-lβ（IL-1β） of mucosa of necrotizing enterocolitis （NEC）, and the activation and intracellular distribution of NF-κB induced by ITF and its role in pathogenesis of NEC in mice. Methods Fifty Wistar mice, one day after birth were equally divided into five groups., the normal control group, normal control ＋ ITF group, NEC model group, NEC ＋ normal saline 0. 2ml subcutaneous injection group, and NEC ＋ ITF group. The mice were fed as normal for three-day and killed on the 4th day The ileocecum were obtained for histological examination by HE staining and the NF-κB level , and the contents of IL- 1β were measured by immunohistochemistry and ELISA assay respectively. Results The contents of IL-1β were obvious increased in NEC models with strong NF-κ B （P65） expression. The models with ITF injection were resulted in marked decrease in IL-1βand NF-B. Conclusions The NF-κB signal route may play important roles in the predisposing factors and signal transduction of NEC. ITF may protect the mucosa by inhibition from the NF-κB signal transduction route in mice.