基于LC-MS的轻、重症急性胰腺炎差异的血清代谢组学研究

Objective: To explore the differential metabolites of mild acute pancreatitis and severe acute pancreatitis, and to provide new ideas for the pathogenesis and treatment of acute pancreatitis transition from mild to severe. Methods: Collect 68 serum specimens of acute pancreatitis diagnosed during hospitalization from Hunan Provincial People's Hospital from August 2020 to March 2021. According to the RAC classification, they were divided into mild acute pancreatitis (40 cases) and severe acute pancreatitis (28 cases). ), using LC-MS metabolomics to analyze the different metabolites and metabolic pathways between the two groups. Results: PCA and PLS-DA analysis showed that the metabolic profile of mild acute pancreatitis was significantly different from that of severe acute pancreatitis. Combining VIP>1, FC>1.5, and P0.9, namely: 2-phenyl-1,3-propanediol monocarbamate, diphenhydramine N-glucaldehyde Acid, rac-5,6-epoxy-retinoyl--D-glucuronic acid, hexafluoroisopropanol, NNAL-N-glucuronic acid, erythritol tetranitrate, 3-hydroxybutyric acid, Tetrahydrodeoxycorticosterone. Among them, the expression elevated in patients with severe pancreatitis are: 2-phenyl-1,3-propanediol monocarbamate rac-5,6-epoxy-retinoyl--D-glucuronic acid, six Fluoroisopropanol, erythritol tetranitrate, 3-hydroxybutyric acid, tetrahydrodeoxycorticosterone, the expression down-regulated are: diphenhydramine N-glucuronic acid, NNAL-N-glucuronide. Conclusion: The metabolites of mild acute pancreatitis and severe acute pancreatitis have changed significantly, including 2-phenyl-1,3-propanediol monocarbamate, diphenhydramine N-glucuronic acid, rac-5,6 -Epoxy-retinoyl--D-glucuronic acid, hexafluoroisopropanol, NNAL-N-glucuronic acid, erythritol tetranitrate, 3-hydroxybutyric acid, tetrahydrodeoxycorticosterone may be Potential biomarkers between the two.