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Ischemia-reperfusion injury(IRI), described as tissue damage caused by reversible ischemic injury or hypoxia prior to the blood supply restoration, is a common pathological phenomenon. In recent study, a hypoxia-reoxygenation (H/R) in the presence or absence of propofol posthypoxia treatment (P-PostH) cell model was built to simulate the condition of IRI, and researchers found propofol may protect cells by suppressing autophagic cell death.To investigate the mechanism underling the protective effect of propofol. A metabolomic analysis was performed in this study using ultra performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF- MS) to compare the metabolism during the process of H/R in the presence or absence of P-PostH. A total of 22 metabolites were detected varied after propofol posthypoxia treatment. Pathway analysis revealed these metabolites were mainly involved in the purine metabolic pathway, three carboxylic acid metabolic pathways, alanine, aspartate and glutamate metabolism pathway and lipid metabolism pathway. We measured the level of Hypoxanthine to verify the metabolomics work, for pathway analysis, we detect the level of reactive oxygen species with H/R and P-PostH treatment. Our study achieved a global comparison of metabolism profiling of H/R cell model with or without propofol posthypoxic treatment. The result indicated that propofol can attenuate endothelial injury caused by IRI by reducing oxidative damage.