我们旨在评估从人参中提取的一种新化合物对人卵巢癌细胞迁移和人脐静脉内皮细胞（HUVECs）形成管状结构的抑制作用。从人参根中分离出一种新的化合物人参内酯 A (1)，并附带七种已知化合物（2-8）。采用光谱数据阐明了化合物1的化学结构。采用 Mayer's hematoxylin 染色评估了 HUVECs 的管状结构形成情况。利用 scratch wound healing 实验评估了 A2780 细胞的迁移。 与其他化合物 2-8 处理的 HUVECs 相比，处理1的 HUVECs 显著减少了管状结构的形成。联合使用磷脂酰肌醇3-激酶（PI3K）（LY294002）和细胞外受体调节激酶（ERK）（U0126）抑制剂可增强该作用。处理1降低了 ERK、PI3K、血管内皮生长因子受体2（VEGFR2）、Akt 和哺乳动物雷帕霉素靶蛋白(mTOR)的磷酸化水平。此外，A2780 细胞在划痕区域的覆盖能力也降低。联合使用 U0126 抑制剂可增强该作用。最后，处理1降低了 ERK、基质金属蛋白酶-9 (MMP-9) 和 MMP-2 的磷酸化水平。这些结果表明人参内酯 A 是一种潜在的 HUVEC 管状结构形成和 A2780 细胞迁移抑制剂，有助于理解其抗癌机制。 © 2022 韩国人参学会。由 Elsevier B.V. 提供的出版服务。

Here, we aimed to assess the inhibitory effect of a new compound from Panax ginseng on the migration of human ovarian cancer cells and tube formation of human umbilical vein endothelial cells (HUVECs).A new compound, ginsenglactone A (1), was isolated from ginseng roots, together with seven known compounds (2-8). Spectroscopic data were used to elucidate the chemical structure of 1. The tubular structure formation in HUVECs was assessed by Mayer's hematoxylin staining. The migration of A2780 cells was evaluated using the scratch wound healing assay.HUVECs treated with 1 had the statistically significant decrease in tubular structure formation compared to the HUVECs treated with compounds 2-8. This effect was enhanced by co-treatment with inhibitors for phosphatidylinositol 3-kinase (PI3K) (LY294002) and extracellular signal-regulated kinase (ERK) (U0126). Treatment with 1 decreased the expression of phosphorylation of ERK, PI3K, vascular endothelial growth factor receptor2 (VEGFR2), Akt, and mammalian target of rapamycin (mTOR). In addition, the ability of A2780 cells to cover the scratched area were also decreased. This effect was enhanced by co-treatment with U0126. Lastly, treatment with 1 decreased the phosphorylation of ERK, matrix metalloproteinase-9 (MMP-9), and MMP-2.These results suggest that ginsenglactone A is a potential inhibitor of HUVEC tubular structure formation and A2780 cellular migration, which may be helpful for understanding its anticancer mechanism.© 2022 The Korean Society of Ginseng. Publishing services by Elsevier B.V.