肠三叶因子对坏死性小肠结肠炎新生大鼠白细胞介素-1β的影响

Influence of Intestinal Trefoil Factor on Interleukin-1β in Neonatal Rats with Necrotizing Enterocolitis

目的探讨肠三叶因子(ITF)对坏死性小肠结肠炎(NEC)新生大鼠肠黏膜组织IL-1β水平的影响,分析ITF对NEC的保护作用。方法50只新生鼠随机分为5组,每组10只:A组为正常对照组,未进行缺氧、低温处理和注射药物;B组为正常ITF组,予皮下注射ITF0.2 mg(0.2 mL);C组为NEC模型组,建立NEC模型后未予药物注射;D组为NEC加9 g/L盐水(NS)组,建立NEC模型后予皮下注射NS0.2 mL;E组为NEC加ITF组,建立NEC模型后予皮下注射ITF0.2 mg(0.2 mL)。第4天断头处死动物后取其回盲部肠组织1～2 cm固定、包埋,HE染色行病理学检查,其他肠道组织制备组织匀浆取上清液应用ELISA试剂盒检测IL-1β水平。结果病理切片示C、D组HE染色切片见肠壁损伤轻重不一,可见全肠黏膜绒毛坏死,病理组织学积分为2～4分,E组肠上皮细胞有少量脱落,顶端绒毛坏死,病理组织学积分为0～2分。C、D组组织匀浆IL-1β水平均较E组显著增高(Pa<0.01);E组与A、B组比较均无显著性差异(Pa>0.05)。结论ITF可通过降低IL-1β的水平减轻NEC模型的肠道炎性反应,ITF有可能为NEC的治疗提供新方法。

Objective To explore the influence of intestinal trefoil factor （ITF） on interleukin - 1β （ IL - 1β） in neonatal rats with necrotizing enteroeofitis（NEC） , and to discuss its protective mechanism for NEC. Methods Fifty rats were randomly assigned into 5 groups, group A（without treatment） as control group;group B as ITF 0.2 mg（0. 2 mL） group,group C as NEC group,group D as NEC plus NS 0.2 mL group,group E as NEC plus ITF 0.2 mg（0.2 mL） group. After NEC model in neonatal rats were established,intestinal tissue within the boundary of ileum and cecum （ 1 - 2 cm） were harvested on the fourth day to observe histological changes. Other inteasinal tissue were treated into homogenate and then were centrifuged. Supernates were used to test the density of IL - 1β by enzyme linked immunosorbent assay （ELISA）. Results Severe intestinal tissue necrosis were observed in the pathological sections of group C and group D with pathological score from 2 to 4. While slight lesions were observed in group E with pathological score from 0 to 2. The level of IL - 1β in group C and group D were significantly higher than that in group E （Pa 〈0.01 ） and there was no significant difference of IL - 1β among group E,A and group B （Pa 〉 0.05 ）. Conclusions ITF can be used to ameliorate instestinal inflammation by decreasing level of IL - 1β,which may provide a new method for the management of NEC.