To clarify the metabolic changes induced by Eurycomanone (EN) in inhibiting the growth and development of Helicoverpa armigera larvae. In this study, the effects of EN, as well as carbohydrates, proteins, and lipids, on the growth and development of H. armigera were examined adopting mixed toxic feed. Furthermore, non-targeted metabolomics techniques were employed to annotate, screen, classify, and analyze the differential metabolites in H. armigera larvae after EN treatment. The results of the growth and development experiment showed that 10 μg/g of EN significantly inhibited the growth and development of H. armigera larvae, with a 2.32-fold decrease in larval weight, a 1.35-fold decrease in pupal weight, and a 33.82% and 29.68% decrease in pupation rate and eclosion rate, respectively. The addition of pancreatic protein hydrolysate and sucrose partially restored the inhibitory activity of EN, while the addition of glycerol had no significant effect on inhibitory activity of larval growth and development. A total of 19 differential metabolites were screened using non-targeted metabolomics techniques, including 11 upregulated and 8 downregulated metabolites, mainly distributed in nutritional metabolic pathways related to amino acids and their metabolites, nucleotides, fatty acyls, and carbohydrates. Among them, Methanesulfonic acid, Methionine sulfoxide, 3-O-Methyldopa, and 3, 4-Dihydroxybenzeneacetic acid were upregulated more significantly, with fold changes of 119.80, 3.34, 2.40, and 2.38, respectively, compared to those of the control group. On the other hand, L-Methionine, Octadecadienamide, L-Tartaric acid, ATP, CTP, β-D-furanfructosyl-α-D-glucopyranoside, Eritadenine, and L-Dopa were down-regulated, with fold changes of 0.49, 0.48, 0.48, 0.41, 0.36, 5.41 × 10^-3, 1.30 × 10^-3 and 1.48 × 10^-4, respectively. This study elucidated the metabolic regulatory mechanism underlying the inhibition of H. armigera growth and development by EN, providing a theoretical basis for the development and utilization of this compound.

To clarify the impact of dicoumarin (DIC) on the ovarian cells metabolome 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 obvious 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 respectively, DIC enhanced cell viability. Through non-targeted metabolomics analysis, a total of 393 differential metabolites were obtained, with 364 DIC upregulated and 29 DIC down-regulated compared to those of the control group. More than 50% differential metabolites were distributed in amino acids and their metabolites (48.3%) and glycerophospholipids (14.2%). The differential metabolites were mainly enriched in nutritional metabolic pathway of amino sugar and nucleotide sugar metabolism, unsaturated fatty acid biosynthesis, sugar biosynthesis, starch and sucrose. Among them, the differential metabolites adrenosterone, LPC (12:0/0:0), N, N-dicyclohexylcarbodiimide, and Val-Pro upregulated by 5 833.56, 15.47, 10.26, and 9.94 times, respectively. This study elucidated the metabolic regulatory mechanism of DIC-induced SL-221 cell proliferation and provided a theoretical basis for the development and utilization of this compound.