基于非靶向代谢组学的脑卒中急性期损伤机制研究OACSTPCD

Objective To study the mechanism of acute stroke injury by untargeted metabolomics.Methods A mouse model of middle cerebral artery occlusion was established to simulate post-stroke ischemia-reperfusion injury.High performance liquid chromatography-mass spectrometry was used to analyze the metabonomics of brain tissue samples after stroke.The Kyoto Encyclopedia of Genes and Genomes(KEGG)database and Human Metabolism Database(HMDB)were used to analyze the metabolome results.Results Among the 194 metabolites that changed significantly after stroke(P<0.05 and VIP>1),111 metabolites were up-regulated and 82 metabolites were down-regulated,among which sesamose,glucuronide,glutathione thiol,uric acid and other substances changed significantly(P<0.01).This belong to the following substances:cofactors,lipids,amino acids,nucleotides,monosaccharides,eicosanes,neurotransmitters,etc.KEGG pathway analysis showed that alanine and glutamate metabolism,taurine metabolism,amino sugar and nucleotide sugar metabolism,glycolysis,nucleotide metabolism,purine metabolism pathways were significantly different(-Log10(P value)>3 and impact value>0.15).Conclusion The activities of lipid metabolism,energy metabolism,and nucleotide metabolism change significantly after stroke,which provides a reference for exploring the mechanism of injury and finding intervention targets.