双香豆素抑制SL-221细胞增殖的差异代谢物分析
Differential metabolite analysis of SL-221 cell proliferation inhibited by dicoumarin
  
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中文关键词:  双香豆素  斜纹夜蛾  代谢组学  细胞活性  代谢通路
英文关键词:Dicoumarin  Spodoptera litura  metabonomics  cell viability  metabolic pathways
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WEN Xue-Mei, SHAO Xue-Hua, HE Xiang-Yu, QIN Zi-Xin, LIANG He, XU Yu-Hui, LU Wei  
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中文摘要:
      为明确双香豆素(DIC)对斜纹夜蛾Spodoptera litura卵巢细胞(SL-221)代谢组的影响。本研究采用CCK-8和非靶向代谢组学技术研究双香豆素抑制SL-221细胞增殖的毒理机理。结果表明,双香豆素对SL-221细胞表现出明显的抑制活性,24 h的抑制中浓度为1.60 μg/mL,且呈浓度依赖性;此外,双香豆素分别与SC 79和胰岛素共培养后,均能提升细胞活力;进一步通过非靶向代谢组学技术获得了393个差异代谢物,双香豆素与对照相比上调了364个,下调29个,而50%以上的差异代谢物分布于氨基酸及其代谢物(48.3%)和甘油磷脂类(14.2%)中;差异代谢物富集主要在氨基糖和核苷酸糖的代谢、不饱和脂肪酸的生物合成、糖的生物合成、淀粉和蔗糖等营养代谢途径中;其中,差异代谢产物肾上腺甾酮(Adrenosterone)、LPC(12:0/0:0)、N,N-二环己基碳二亚胺(N,N-dicyclohexylcarbodiimide)和L-缬氨酸-L-脯氨酸(Val-Pro)分别上调了5 833.56倍、15.47倍、10.26倍和9.94倍。本研究解析了双香豆素诱导斜纹夜蛾卵巢细胞增殖的代谢调控机制,为该化合物的开发利用提供了理论依据。
英文摘要:
      To clarify the impact of dicoumarin (DIC) on the metabolic profile ovarian cells of Spodoptera litura (SL-221), this study employed CCK-8 and non-targeted metabolomics techniques to investigate the toxicological mechanism of DIC in inhibiting SL-221 cells proliferation. The results showed that DIC exhibited significant inhibitory activity against SL-221 cells, with an inhibitory concentration of 1.60 μg/mL at 24 h, and the inhibition was concentration-dependent. Furthermore, when co-cultured with SC 79 and insulin, DIC enhanced cell viability. Through non-targeted metabolomics analysis, a total of 393 differential metabolites were obtained, with 364 upregulated and 29 downregulated by DIC compared to the control. More than 50% of the differential metabolites were distributed in amino acids and their metabolites (48.3%) and glycerophospholipids (14.2%). The enriched differential metabolites were mainly involved in amino sugar and nucleotide sugar metabolism, unsaturated fatty acid biosynthesis, sugar biosynthesis, starch and sucrose metabolism, and other nutrient metabolism pathways. Among them, the differential metabolites adrenosterone, LPC (12:0/0:0), N,N-dicyclohexylcarbodiimide, and Val-Pro were upregulated by 5833.56, 15.47, 10.26, and 9.94 times, respectively. This study elucidated the metabolic regulatory mechanism underlying DIC-induced SL-221 cell proliferation and provided a theoretical basis for the development and utilization of this compound.
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