【摘要】 目的:应用代谢组学方法,研究右美托咪啶(DEX)预处理LPS(脂多糖)诱导的巨噬细胞炎症模型代谢物的变化,探讨其抗炎机制可能性代谢途径。方法:DEX预处理LPS诱导的巨噬细胞炎症模型,利用超高效液相色谱-三重四级杆-线性离子阱质谱(UPLC-Q-TRAP-MS/MS)采集细胞代谢物信息,并采用多元变量统计方法:主成分分析法、正交偏最小二乘法判别分析法筛选细胞差异代谢物。结果:与对照组相比,DEX干预后筛选出甜菜碱、胆碱、乳酸、谷氨酰胺、蛋氨酸、S-腺苷L-甲硫氨酸、磷脂酰甘油、磷脂酰胆碱、瓜氨酸、脯氨酸、二磷酸腺苷(ADP)、环磷酸腺苷(c AMP)、丙酮酸等22种差异代谢物。结论:代谢组学方法显示DEX预处理炎症细胞特征性代谢物分子,为DEX抗炎生物机制奠定基础。更多还原

【Abstract】 Objective: To study the influence of dexmedetomidine( DEX) pretreatment on the metabolites in RAW264.7 inflammation model induced by lipopolysaccharide( LPS) in mouse peritoneal macrophages by metabolomics,and explore its regulative approaches. Methods: DEX pre-treated LPS-induced macropflammation model. The metabolites in the cells were analyzed by UPLCQTRAP-MS/MS. The metabolic markers were screened by the principal component analysis( PCA) and orthogonal partial least squares discriminant analysis( OPLS-DA). Results: Compared with the control group,22 differential metabolites were detected out from the DEX-pretreated LPS-induced macrophages,including betaine,choline,lactic acid,glutamine,methionine,S-adenosine-L-methionine,phosphatidyl glycerin,phosphatidyl choline,citrulline,proline,ADP,c AMP and pyruvate. Conclusion: The metabolic markers are screened out in LPS-induced cells pretreated with DEX,and amino acid,glucose,lipid and nucleotide in the related metabolic pathways show significant changes. DEX may exert an anti-inflammatory effect by affecting the changes in the metabolites of metabolic pathways. Metabolomics can show the metabolic markers in LPS-induced cells pretreated with DEX,which lays a foundation for the anti-inflammatory biological mechanism of DEX.更多还原