Lipopolysaccharide (LPS) can lead to uncontrollable cytokine production, fatal sepsis syndrome and depression/multiple organ failure, as pathophysiologic demonstration. Various toxic effects of LPS have been extensively reported, mainly on the toxicity of LPS in cellular level, macrophages or tumor cells, etc. This work aimed on the impact of LPS on mast cell metabolism, which focused on LPS-induced cellular metabolic profiles. Gas chromatography-mass spectrometry (GC-MS) based metabolomics strategy was implemented for the endo-metabolites detection in rat basophilic leukemia (RBL-2H3) cells, treated with 10 μg/mL LPS for 24 h, along with multiple time-dose tests of cells viability/apoptosis. Significantly changes metabolites were mainly involved the metabolism of glycine, serine, threonine and the biosynthesis of phenylalanine, tyrosine, tryptophan and pentose phosphate pathway. The endo-metabolism results illustrated that LPS treatment led to downregulation of glycine, serine and threonine metabolism besides pentose phosphate pathway in RBL-2H3 cells. This novel insight into LPS cellular metabolism, provides some heuristic guidance for elucidating the underlying mechanism of LPS-mediated disease.

脂多糖（LPS）可以导致无法控制的细胞因子产生，致命性败血症综合征和抑郁/多器官衰竭，这是病理生理学证明。LPS的各种毒性作用已被广泛报道，主要是在细胞水平，巨噬细胞或肿瘤细胞等方面对LPS的毒性。这项工作旨在研究LPS对肥大细胞代谢的影响，其研究重点是LPS诱导的细胞代谢谱。实施基于气相色谱-质谱（GC-MS）的代谢组学策略来检测大鼠嗜碱性白血病（RBL-2H3）细胞中的内代谢物，并用10μg/ mL LPS处理24 h，并进行多次时间剂量试验细胞活力/凋亡。代谢物的显着变化主要涉及甘氨酸，丝氨酸，苏氨酸的代谢以及苯丙氨酸，酪氨酸，色氨酸和戊糖磷酸途径。体内代谢结果表明，LPS处理除了使RBL-2H3细胞中的戊糖磷酸途径外，还导致甘氨酸，丝氨酸和苏氨酸代谢的下调。对LPS细胞代谢的这种新颖见解，为阐明LPS介导的疾病的潜在机制提供了一些启发性指导。