Geier Mark S, Butler Ross N, Giffard Philip M, Howarth Gordon S
Centre for Paediatric and Adolescent Gastroenterology, Children, Youth and Women's Health Service, 72 King William Road, North Adelaide, South Australia, Australia.
Dis Colon Rectum. 2007 Jul;50(7):1061-9. doi: 10.1007/s10350-007-0213-x.
Opposing effects of the prebiotic, fructooligosaccharide, have been reported in experimental colitis. We compared the effects of the prebiotic, fructooligosaccharide, alone and in synbiotic combination with Lactobacillus fermentum BR11, on the development of dextran sulfate sodium-induced colitis in rats. Rats consumed an 18 percent casein-based diet or diet supplemented with 6 percent fructooligosaccharide or maltodextrin for 14 days. The synbiotic group was gavaged 1 ml of L. fermentum BR11 (1x10(9) cfu/ml) twice daily. From Days 7 to 14, colitis was induced via 3 percent dextran sulfate sodium in drinking water. Disease activity was assessed daily, and at killing, gastrointestinal organs were measured, weighed, and examined by quantitative histology, proliferating cell nuclear antigen immunohistochemistry, and colonic myeloperoxidase activity. Administration of dextran sulfate sodium resulted in an increased colitic disease activity, and an increased colon and cecum weight compared with normal controls. Colon and cecum weights were further increased in dextran sulfate sodium+fructooligosaccharide (colon: 19 percent; cecum: 48 percent) and dextran sulfate sodium+fructooligosaccharide/L. fermentum BR11-treated rats (16 and 62 percent) compared with dextran sulfate sodium+vehicle-treatment. Dextran sulfate sodium+fructooligosaccharide-treated rats displayed an 81 percent increase in colonic myeloperoxidase activity compared with dextran sulfate sodium-treated controls. Histologic damage severity scores increased in dextran sulfate sodium+vehicle, dextran sulfate sodium+fructooligosaccharide, and dextran sulfate sodium+fructooligosaccharide/L. fermentum BR11-treated rats compared with normal controls (P<0.05). Crypt depth increased in all treatments compared with normal controls (P<0.01). No protection from dextran sulfate sodium-colitis was accorded by fructooligosaccharide alone or in synbiotic combination with L. fermentum BR11, whereas fructooligosaccharide actually increased some indicators of colonic injury.
已报道益生元低聚果糖在实验性结肠炎中有相反的作用。我们比较了单独使用益生元低聚果糖以及将其与发酵乳杆菌BR11以合生元形式联合使用，对葡聚糖硫酸钠诱导的大鼠结肠炎发展的影响。大鼠食用18%的酪蛋白基饮食或补充6%低聚果糖或麦芽糖糊精的饮食14天。合生元组每天两次灌胃1ml发酵乳杆菌BR11（1×10⁹ cfu/ml）。从第7天到第14天，通过在饮用水中添加3%的葡聚糖硫酸钠诱导结肠炎。每天评估疾病活动度，处死时测量、称重胃肠道器官，并通过定量组织学、增殖细胞核抗原免疫组织化学和结肠髓过氧化物酶活性进行检查。与正常对照组相比，给予葡聚糖硫酸钠导致结肠炎疾病活动度增加，结肠和盲肠重量增加。与葡聚糖硫酸钠+赋形剂处理组相比，葡聚糖硫酸钠+低聚果糖组（结肠：19%；盲肠：48%）和葡聚糖硫酸钠+低聚果糖/发酵乳杆菌BR11处理组（16%和62%）的结肠和盲肠重量进一步增加。与葡聚糖硫酸钠处理的对照组相比，葡聚糖硫酸钠+低聚果糖处理的大鼠结肠髓过氧化物酶活性增加了81%。与正常对照组相比，葡聚糖硫酸钠+赋形剂组、葡聚糖硫酸钠+低聚果糖组和葡聚糖硫酸钠+低聚果糖/发酵乳杆菌BR11处理组的组织学损伤严重程度评分增加（P<0.05）。与正常对照组相比，所有处理组的隐窝深度均增加（P<0.01）。单独使用低聚果糖或与发酵乳杆菌BR11以合生元形式联合使用均不能预防葡聚糖硫酸钠诱导的结肠炎，而低聚果糖实际上增加了结肠损伤的一些指标。
