Objective: To study the effect of glutamine-supplemented enteral nutrition in regulating the apoptosis of intestinal mucosal cells and promoting mucosal healing in young rats with inflammatory bowl disease (IBD).
Methods: A total of 80 male Sprague-Dawley rats aged 4-5 weeks were randomly divided into 4 groups: blank control, IBD model, short peptide, and short peptide+glutamine (n=20 each). The IBD model was prepared by a single colon perfusion of 3-nitrobenzene sulfonic acid. At 3 days after modeling, the rats in the short peptide group were fed with short peptide formula (100 mL/kg), and those in the short peptide+glutamine group were fed with short peptide formula (100 mL/kg) and glutamine (0.5 g/kg). The course of intervention was 1 week. General conditions were observed after the experiment and their intestinal mucosal tissue was obtained. Hematoxylin-eosin staining was used to observe the pathological change of the intestinal mucosa. RT-PCR was used to measure the expression of apoptosis-regulating genes (bax and bc1-2) and apoptotic signal transduction factors (Caspase-3 and Caspase-9) in the intestinal mucosa. Western blot was used to measure the expression of insulin-like growth factor-1 (IGF-1) in the colonic mucosa.
Results: The IBD model group had poorer general conditions than the other three groups (blank control, short peptide and short peptide+glutamine), and the short peptide+glutamine group had better general conditions than the IBD model and short peptide groups. The IBD model group had significantly higher mRNA expression of bax than the other three groups (P<0.05). There was no significant difference in the mRNA expression of bcl-2, Caspase-3 and Caspase-9 among the 4 groups (P>0.05). The short peptide group had a significantly higher level of IGF-1 than the short peptide+glutamine, blank control and IBD model groups (P<0.05).
Conclusions: Glutamine-supplemented enteral nutrition can effectively improve the general nutritional status of young rats with IBD, but it is not better than exclusive enteral nutrition in inhibiting the apoptosis of colonic mucosal cells and stimulating the synthesis of IGF-1 in the intestinal mucosa.
目的: 探讨谷氨酰胺强化肠内营养对炎症性肠病（IBD）幼鼠模型肠黏膜细胞凋亡的调控及促进黏膜愈合的作用。
方法: 将80只4~5周龄Sprague-Dawley雄性大鼠随机分为空白对照组、IBD模型组、短肽组和短肽+谷氨酰胺（Gln）组，每组20只。采用一次性结肠灌注三硝基苯磺酸建立IBD模型，造模3 d后，短肽组给予短肽制剂（100 mL/kg），短肽+Gln组给予短肽制剂（100 mL/kg）+Gln（0.5 g/kg），干预1周。实验结束后观察幼鼠的一般情况，并留取肠黏膜，苏木素-伊红（HE）染色观察肠黏膜组织病理情况；RTPCR法检测肠黏膜凋亡调控基因（bax、bcl-2）及凋亡信号转导因子（Caspase-3、Caspase-9）的表达；Westernblot法检测结肠黏膜IGF-1表达水平。
结果: IBD模型组一般情况均较其他组差，短肽+Gln组一般情况优于IBD模型组和短肽组。模型组bax mRNA表达水平高于空白对照组、短肽组和短肽+Gln组（P < 0.05）；bcl-2、Caspase-3、Caspase-9 mRNA水平在各组比较差异均无统计学意义（P > 0.05）。短肽组IGF-1水平明显高于短肽+Gln组、空白对照组及IBD模型组（P < 0.05）。
结论: Gln强化肠内营养能有效改善IBD模型幼鼠的一般营养状况，但在抑制结肠黏膜细胞凋亡及刺激结肠黏膜IGF-1合成方面并未优于专一肠内营养。