首页> 美国卫生研究院文献>Saudi Journal of Biological Sciences >Metabonomics of mice intestine in Codonopsis foetens induced apoptosis of intestine cancer cells
【2h】

Metabonomics of mice intestine in Codonopsis foetens induced apoptosis of intestine cancer cells

机译:党参小鼠肠道的代谢组学诱导肠癌细胞凋亡。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Intestinal cancer is a disease with high morbidity and high mortality in China. Previous studies have shown that Codonopsis foetens can inhibit cellular autophagy and promote the apoptosis of intestine cancer cells. Based on metabolomics method coupled with liquid chromatography-mass spectrometry (LC-MS) technology, we aimed to analyze intestinal small molecule metabolites in the intestinal cancer model group and the Codonopsis foetens treated group. Principal component analysis (PCA) and Partial Least Squares (PLS-DA) were used to identify the pattern of the data. And the metabolic characteristics of the cancer model group were explored based on the metabolic differences between the groups. Multivariate statistical analysis revealed that metabolites presented with differences included: Acetamide, Phosphoric acid, Hydrogen sulfite, Pyruvic acid, Cytosine, 2-Hydroxypyridine, Phosphoric acid, Uracil, Gamma-Aminobutyric acid, Glycerol alpha-monochlorohydrin, Thiosulfic acid, L-Valine, Cysteamine, Taurine, Creatine, Homocysteine, Hypoxanthine, Se-Methylselenocysteine, 5-Hydroxymethyluracil, Oxoglutaric acid, LysoPC(20:0), LysoPC(22:4(7Z,10Z,13Z,16Z)), LysoPC(18:2(9Z,12Z)), LysoPC(16:1(9Z)), LysoPE(0:0/16:0), LysoPE(0:0/18:2(9Z,12Z)), LysoPE(18:0/0:0), LysoPE(20:1(11Z)/0:0), etc. Combined with metabolic pathway analysis, pathways presented with differences included: Citrate cycle (TCA cycle), ABC transporters, 2-Oxocarboxylic acid metabolism, Taurine and hypotaurine metabolism, Butanoate metabolism), Phenylalanine, tyrosine and tryptophan biosynthesis, Biosynthesis of amino acids, Protein digestion and absorption, Aminoacyl-tRNA biosynthesis, C5-Branched dibasic acid metabolism, GABAergic synapse, Proximal tubule bicarbonate reclamation, Mineral absorption, Phenylalanine metabolism. The results showed that the proliferation of intestinal cancer cells caused cell metabolism disorders, manifesting as changes in metabolic pathways and resulting in changes in metabolites.
机译:在中国,肠癌是高发病率和高死亡率的疾病。先前的研究表明,党参能抑制细胞自噬并促进肠癌细胞的凋亡。基于代谢组学方法,结合液相色谱-质谱(LC-MS)技术,我们旨在分析肠癌模型组和党参治疗组中的肠小分子代谢产物。主成分分析(PCA)和偏最小二乘(PLS-DA)用于识别数据模式。根据癌症模型组之间的代谢差异,探索其代谢特征。多变量统计分析显示,存在差异的代谢物包括:乙酰胺,磷酸,亚硫酸氢盐,丙酮酸,胞嘧啶,2-羟基吡啶,磷酸,尿嘧啶,γ-氨基丁酸,甘油α-一氯代醇,硫代硫酸,L-缬氨酸,半胱胺,牛磺酸,肌酸,同型半胱氨酸,次黄嘌呤,硒甲基硒代半胱氨酸,5-羟甲基尿嘧啶,氧戊二酸,LysoPC(20:0),LysoPC(22:4(7Z,10Z,13Z,16Z)),LysoPC(18:2( 9Z,12Z)),LysoPC(16:1(9Z)),LysoPE(0:0/16:0),LysoPE(0:0/18:2(9Z,12Z)),LysoPE(18:0/0 :0),LysoPE(20:1(11Z)/ 0:0)等。结合代谢途径分析,所呈现的途径有所不同,包括:柠檬酸循环(TCA循环),ABC转运蛋白,2-氧代羧酸代谢,牛磺酸和牛磺酸,丁酸代谢),苯丙氨酸,酪氨酸和色氨酸的生物合成,氨基酸的生物合成,蛋白质的消化吸收,氨酰基-tRNA的生物合成,C5-分支的二元酸代谢,GABA能突触,近端小管碳酸氢盐回收,矿物质吸收,苯丙氨酸代谢。结果表明,肠癌细胞的增殖引起细胞代谢紊乱,表现为代谢途径的改变并导致代谢物的改变。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号