Ann Ji Yong, Kim Sang Jung, Han Sang Pyo, Kim Jeong Wook, Kim Hyung Joon, Do Jae Hyuk, Kim Jae Gyu, Chang Sae Kyung, Jeon Woo Kyu
Department of Internal Medicine, Chungang University College of Medicine, Seoul, Korea.
Korean J Gastroenterol. 2004 Nov;44(5):252-8.
BACKGROUND/AIMS: NSAIDs induce gut damage throughout the entire gastrointestinal tract and bacterial translocation. The aim of this study was to examine if administration of glutamine was able to prevent the NSAID-induced gut damages and bacterial translocation in the animal models.
Rats were utilized into 5 groups; control group, diclofenac group, and diclofenac with glutamine 0.8, 1.6, and 3.2 g/kg/day group. The animals with glutamine were fed with L-glutamine for 4 days before diclofenac administration. Gut injury was induced by administration of a single dose of diclofenac (80 mg/kg orally). Intestinal permeability (24 hour urinary excretion of phenolsulfonphthalein), enteric aerobic bacterial counts, serum biochemical profiles and bacterial translocation to mesenteric lymph nodes, liver and spleen were measured.
Diclofenac caused the increase in intestinal permeability, enteric bacterial count, enteric protein and albumin loss and bacterial translocation. Administration of glutamine reduced the increase in intestinal permeability, protein losing enteropathy, enteric bacterial overgrowth and bacterial translocation induced by diclofenac.
Glutamine may have beneficial effects on NSAID-induced gut damage and bacterial translocation.
背景/目的：非甾体抗炎药（NSAIDs）可导致全胃肠道损伤及细菌移位。本研究旨在探讨给予谷氨酰胺是否能够预防动物模型中NSAIDs诱导的肠道损伤及细菌移位。
将大鼠分为5组；对照组、双氯芬酸组以及双氯芬酸与0.8、1.6和3.2 g/kg/天谷氨酰胺合用组。给予谷氨酰胺的动物在给予双氯芬酸前4天喂食L-谷氨酰胺。通过单次口服双氯芬酸（80 mg/kg）诱导肠道损伤。测定肠道通透性（酚红24小时尿排泄量）、肠道需氧菌计数、血清生化指标以及细菌向肠系膜淋巴结、肝脏和脾脏的移位情况。
双氯芬酸导致肠道通透性增加、肠道细菌计数增加、肠道蛋白质和白蛋白丢失以及细菌移位。给予谷氨酰胺可减轻双氯芬酸诱导的肠道通透性增加、蛋白丢失性肠病、肠道细菌过度生长及细菌移位。
谷氨酰胺可能对NSAIDs诱导的肠道损伤及细菌移位具有有益作用。
