Shi Lei, Zhang Bing-Hong, Yu Hong-Gang, Yu Jie-Ping, Xi Juan-Li
Department of Gastroenterology, Renmin Hospital of Wuhan University, 430060 Wuhan, PR China.
J Perinat Med. 2007;35(5):443-6. doi: 10.1515/JPM.2007.096.
Neonatal necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants. The role of cytokines and growth factors in the pathophysiology of NEC is not yet clearly defined. Among these factors, the intestinal trefoil factor (ITF) is known as cytoprotective to the gut. We studied the cytoprotective effect of trefoil factor in the 1-day-old Wistar rat pup model following hypoxic-ischemic cold stress.
In the present study, thirty 1-day-old Wistar rat pups were randomly divided into three groups: Group 1, normal controls: Group 2, NEC; Group 3, NEC+ITF. Experimental NEC was induced by exposure to hypoxia for 60 s followed by cold stress at 4 degrees C for 10 min. The animals were euthanized at development of NEC, and at 96 h the intestinal tissue was processed and examined for histological changes of NEC.
The pathological lesions indicated severe separation of the submucosa and lamina propria and tissue necrosis in Group 2, and slight submucosal and lamina propria separation in Group 3. There were no histopathological changes in the controls. The mean of histological grade of group 2 was 2.8 (range 2-4), and 1.2 (range 0-2) in group 3. A difference was found when the two groups were compared (P<0.05).
ITF may provide a new way for the therapy of NEC in rats.
新生儿坏死性小肠结肠炎(NEC)是早产儿最常见的胃肠道疾病。细胞因子和生长因子在NEC病理生理学中的作用尚未明确界定。在这些因素中,肠三叶因子(ITF)被认为对肠道具有细胞保护作用。我们研究了三叶因子在1日龄Wistar大鼠幼崽缺氧缺血性冷应激模型中的细胞保护作用。
在本研究中,30只1日龄Wistar大鼠幼崽被随机分为三组:第1组,正常对照组;第2组,NEC组;第3组,NEC+ITF组。通过暴露于缺氧60秒,随后在4℃冷应激10分钟诱导实验性NEC。在NEC发生时对动物实施安乐死,并在96小时时对肠道组织进行处理,检查NEC的组织学变化。
病理病变显示,第2组黏膜下层和固有层严重分离且组织坏死,第3组黏膜下层和固有层有轻微分离。对照组无组织病理学变化。第2组组织学分级的平均值为2.8(范围2-4),第3组为1.2(范围0-2)。两组比较时发现有差异(P<0.05)。
ITF可能为大鼠NEC的治疗提供一种新方法。