中文摘要：

研究乳源酪蛋白糖巨肽（casein glycomacropeptide,CGMP）对溃疡性结肠炎（ulcerative colitis,UC）小鼠肠道菌群多样性的影响,从肠道菌群角度探讨乳源CGMP改善溃疡性结肠炎与肠道菌群变化关系的可能机制。恶唑酮（oxazolone,OXZ）诱导小鼠UC模型,设立正常对照组、模型对照组、乳源CGMP组（50 mg/（kg·d））和柳氮磺胺吡啶（salazosulfapyridine,SASP）治疗组（40 mg/（kg·d））,其中正常对照组和模型对照组灌胃相应剂量的生理盐水,连续灌胃7 d。利用Ion Torrent PGM技术检测实验期间小鼠肠道菌群多样性的变化。UC小鼠肠道菌群结构失调,其肠道菌群多样性降低以及优势菌群比例下降。对测序序列通过主成分分析（principal component analysis,PCA）、Uni Frac等统计分析发现,UC小鼠肠道中厚壁菌门（Firmicutes）和拟杆菌门（Bacteroidetes）的丰度降低而放线菌门（Actinobacteria）和变形菌门（Proteobacteria）的丰度升高。乳源CGMP干预后UC小鼠肠道菌群多样性增加,厚壁菌门和拟杆菌门的相对比例高于模型组,提示乳源CGMP可通过调节失衡的肠道菌群来改善UC。

英文摘要：

In order to investigate the modulation of casein glycomacropeptide（CGMP） on the diversity of intestinal flora in mice with ulcerative colitis（UC）, an oxazolone-induced mouse model with ulcerative colitis was used to explore the intestinal flora in the presence of CGMP and the mechanism underlying the treatment of ulcerative colitis through CGMP. The mice with oxazolone-induced ulcerative colitis were divided into four groups including normal control group, model control group, CGMP group and salazosulfapyridine（SASP） group. After oxazolone challenge, the mouse in model control group were given regular feed as same as that provided to normal control group, and the mice in CGMP group and SASP group were administrated with CGMP at 50 mg/（kg·d） and SASP at 40 mg/（kg·d） for 7 consecutive days. Ion Torrent sequencing technology was applied to detect the diversity of intestinal flora in mice. Marked structural changes were discovered in the gut microbiota of mice with ulcerative colitis, showing a reduction in intestinal flora diversity and decline in dominant bacterial populations. The sequencing data were analyzed by multivariate statistical methods and the results showed that the abundance of Bacteroidetes and Firmicutes were significantly decreased, whereas Actinobacteria and Proteobacteria were increased. The intestinal bacterial diversity in UC mice was increased after the intervention of CGMP, indicating that CGMP could improve the oxazolone-induced ulcerative colitis of mice by adjusting the imbalanced intestinal flora.