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目的:以药物干预前后的Jurkat细胞为样本,旨在找出能够有效干预淋巴瘤的药物及与淋巴瘤相关的代谢及信号通路。方法:以UPLC-3Q MS为技术平台,通过多反应监测(Multiple Reaction Monitoring,MRM)扫描模式,根据实验室前期淋巴瘤代谢组学的研究成果,选择对淋巴瘤患者和健康对照组分类有显著贡献的脂类差异代谢物作为监测对象,对PI3K inhibitor干预前后的Jurkat细胞内这些潜在的生物标记物进行定量研究。结果:PI3K inhibitor与Jurkat细胞作用一段时间后,所监测的四个脂质代谢物含量呈现出与药物干预前肿瘤组相反的变化趋势,药物干预后细胞内含量有明显先升高再降低的趋势。结论:说明PI3K介导的信号通路在淋巴瘤细胞内被放大,选择性抑制该通路可以有效抑制肿瘤增殖和肿瘤细胞的代谢活动,为淋巴瘤的临床研究提供依据。
OBJECTIVE: To identify Jurkat cells before and after drug intervention in order to find out the drugs that can effectively interfere with lymphoma and the metabolism and signal pathways related to lymphoma. Methods: The UPLC-3Q MS was used as a technology platform to select patients with lymphoma and healthy controls according to the research results of metabonomics of pre-laboratory lymphoma through multiple reaction monitoring (MRM) The contribution of lipid differential metabolites was monitored as a quantitative study of these potential biomarkers in Jurkat cells before and after PI3K inhibitor intervention. RESULTS: After a period of treatment with PI3K inhibitor and Jurkat cells, the contents of the four lipid metabolites monitored showed the opposite trend as that before the drug intervention. The intracellular content of PI3K inhibitor increased significantly and then decreased . Conclusion: PI3K-mediated signaling pathway is amplified in lymphoma cells, and selective inhibition of this pathway can effectively inhibit tumor proliferation and tumor cell metabolic activity, providing a basis for the clinical study of lymphoma.