摘要
目的探究高尿酸血症轻度认知功能障碍模型大鼠肠道菌群的变化。方法给予大鼠含有2%尿酸和2%氧嗪酸钾的高尿酸复合饲料12周,构建高尿酸血症轻度认知功能障碍模型。采用Morris水迷宫、血生化等指标对模型进行评价,并利用16S rDNA测序研究该模型的肠道菌群变化。结果与对照组相比,模型大鼠血清尿酸明显升高,逃逸潜伏期明显延长,以及目标象限停留时间明显缩短。且模型大鼠肠道菌群多样性发生改变,14种菌群的相对丰度显著变化,结论尿酸持续性升高可诱导肠道菌群结构失衡,而肠道菌群失调与轻度认知功能障碍的发生发展密切相关,可能是高尿酸血症轻度认知功能障碍的机制之一。
Aim To explore changes of gut microbiota in experimental model rats with hyperuricemia-induced mild cognitive impairment.Methods The experimental rats were provided with a diet containing 2%W/W uric acid(UA)and 2%W/W oxonic acid for period ranging from 1 day to 12 weeks.Morris water maze,blood biochemical indexes and other auxiliary models were used to evaluate the experimental animal model.Changes of gut microbiota were studied by 16S rDNA high-throughput sequencing.Results Compared with control group,the amount of UA of rats was significantly elevated.In addition,the rats showed significantly reduced spatial learning and memory in an escape latency and probe trial.The diversity of gut microbiota in model rats changed,and the relative abundances of 14 species of gut microbiota changed markedly.The abundance of Butyrivibrio,Erysipelotrichia,Erysipelotrichales,Erysipelotrichaceae,Erysipelatoclostridium,Lachnoclostridium 5,Anaeroplasmatales,Anaeroplasmataceae and Anaeroplasma in model mice increased,while that of Dorea,RuminococcaceaeUCG_005,Butyricicoccus,Tyzzerella 3 and Parasutterella decreased.Conclusions The continuous increase of UA can regulate gut microbiota,and the imbalance of gut microbiota is closely related to the development of mild cognitive impairment,which may be one of the mechanisms of hyperuricemia-induced mild cognitive impairment.
作者
穆卡然·艾买江
吴美薇
李娜
何彭可
李佳川
邵晓妮
AIMAIJIANG Mukaran;WU Mei-wei;LI Na;HE Peng-ke;LI Jia-chuan;SHAO Xiao-ni(College of Pharmacy, Southwest Minzu University, Chengdu 610041, China)
出处
《中国药理学通报》
CAS
CSCD
北大核心
2021年第11期1599-1606,共8页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No81801086)
西南民族大学中央高校基本科研业务费专项资金资助项目(No2019HQZZ19)。
