| 引用本文: |
钟森杰,李静,黄淑敏,杨梦,邱宏,程彬,胡志希,李琳.慢性心衰心气阴虚证模型大鼠的粪便代谢组学研究[J].湖南中医药大学学报,2020,40(6):660-665[点击复制] |
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| 慢性心衰心气阴虚证模型大鼠的粪便代谢组学研究 |
| 钟森杰,李静,黄淑敏,杨梦,邱宏,程彬,胡志希,李琳 |
| (湖南中医药大学中医诊断研究所, 湖南 长沙 410208) |
| 摘要: |
| 目的 研究慢性心衰心气阴虚证大鼠的粪便代谢组学特征。方法 13只Dahl盐敏感大鼠随机分为空白对照组(6只)和模型组(7只)，以高盐饲料(8% NaCl)饲养模型组大鼠20周复制心衰模型。成模后采集两组大鼠的粪便样本，运用超高效液相色谱-质谱(UPLC-MS)联用技术和多元统计分析其代谢成分。结果 主成分分析和偏最小二乘判别分析得到的得分图显示，两组的代谢成分积分点完全分离，表明两组大鼠的代谢模式存在明显差异。与空白对照组比较，模型组神经氨酸、尿苷、丙氨酰色氨酸、酪氨酰缬氨酸、苯丙氨酰甘氨酸、牛磺脱氧胆酸、粪甾烷酸、白三烯E4的水平上调，谷氨酸、酪氨酸、烟酸、鞘氨醇、二十四烷酸、二十二碳六烯酸、亚油酸的水平下调。15种差异代谢产物参与了19条代谢通路，其中氮代谢通路和氨酰tRNA的生物合成通路富集性较显著。结论 慢性心衰心气阴虚证大鼠的代谢功能异常，其病理机制涉及氨基酸代谢紊乱、蛋白质代谢紊乱、脂代谢紊乱、炎症反应、肠道功能失衡等多个层面。 |
| 关键词: 慢性心衰 心气阴虚证 代谢组学 |
| DOI：10.3969/j.issn.1674-070X.2020.06.004 |
| 投稿时间：2019-09-27 |
| 基金项目:国家自然科学基金项目（81774208）；湖南省自然科学基金项目（2019JJ50447）；湖南省教育厅优秀青年项目（18B235）。 |
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| Study on Fecal Metabolomics of Heart-Qi Yin Deficiency Syndrome Model Rats of Chronic Heart Failure |
| ZHONG Senjie,LI Jing,HUANG Shumin,YANG Meng,QIU Hong,CHENG Bin,HU Zhixi,LI Lin |
| (Diagnostic Institute of Hunan University of Chinese Medicine, Changsha, Hunan 410208, China) |
| Abstract: |
| Objective To study the fecal metabolomic characteristics of rats with heart-Qi Yin deficiency syndrome of chronic heart failure. Methods Thirteen Dahl salt-sensitive rats were divided into a blank control group (6 rats) and a model group (7 rats). Rats in the model group were fed with high salt diet (8% NaCl) for 20 weeks to replicate the heart failure model. After modeling, fecal samples from the 2 groups of rats were collected, and their metabolic components were analyzed using ultra-high performance liquid chromatography-mass spectrometry (UPLC-MS) combined technology and multivariate statistical analysis. Results The score chart obtained by principal component analysis and partial least squares-discriminant analysis showed that the integral point of metabolic components was completely separated between the 2 groups, indicating that there was a significant difference in metabolic pattern between the 2 groups. Compared with the blank control group, the levels of neuraminic acid, uridine, alanyl tryptophan, tyrosinyl valine, phenylalanyl glycine, taurodeoxycholic acid, coprocholic acid and leukotriene E4 in the model group were up-regulated. The levels of glutamic acid, tyrosine, nicotinic acid, sphingosine, tetracarboxylic acid, docosahexaenoic acid and linoleic acid were down-regulated. 15 different metabolites participated in 19 metabolic pathways. Nitrogen metabolism pathway and aminoacyl-tRNA biosynthesis pathway had more significant enrichment. Conclusion Metabolic function of rats with heart-Qi Yin deficiency syndrome of chronic heart failure was disturbed. Its pathological mechanism involves amino acid metabolism disorder, protein metabolism disorder, lipid metabolism disorder, inflammatory reaction, intestinal dysfunction and other aspects. |
| Key words: chronic heart failure heart-Qi Yin deficiency syndrome metabolomics |
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