[摘要] 目的:探索人参皂苷Rg3 体外对胃癌SGC7901 细胞血管生成拟态（VM）形成的影响及其分子机制。方法: MTT法检测不同浓度Rg3 对SGC7901 细胞增殖的影响；SGC7901 细胞分为BML-284 组、XAV-939 组、Rg3 组、Rg3+BML-284 组和空白组，Transwell 实验检测细胞的侵袭和迁移，成管实验观察细胞管样结构的形成，ELISA检测细胞MMP-9 和MMP2 分泌变化，qPCR检测细胞中GSK-3β、Wnt2B mRNA表达水平，WB检测细胞中β 联蛋白表达水平，免疫荧光检测β 联蛋白进入细胞核情况。结果：人参皂苷Rg3 可以时间-浓度依赖的方式抑制SGC7901 细胞增殖。与空白组相比，40 mg/L Rg3 显著抑制SGC7901 细胞侵袭和迁移（均P<0.05）、VM的形成（P<0.05），同时细胞中GSK-3β、Wnt2B mRNA和β 联蛋白的表达及其进核行为均受到显著抑制（均P<0.05）；Rg3+BML-284 组细胞的侵袭、迁移以及VM的形成情况与空白组无显著差异（均P>0.05）。结论: Rg3 通过抑制SGC7901细胞中Wnt/β 联蛋白通路激活从而抑制细胞的侵袭、迁移以及VM的形成。

[Abstract] Objective: To investigate the effects of ginsenoside Rg3 on the formation of vasculogenic mimicry (VM) in gastric cancer cell line SGC7901 and its molecular mechanism. Methods: MTT assay was used to detect the effect of different concentrations of Rg3 on the proliferation of SGC7901 cells. SGC7901 cells were grouped as follows: BML-284 group, XAV-939 group, Rg3 group, Rg3+BML-284 group and blank group. Transwell chamber assay was used to detect cell invasion and migration; the formation of VM was observed by tube formation assay; the secretion of MMP-9 and MMP2 was detected by ELISA; the mRNA expressions of GSK-3β and Wnt2B were detected by qPCR; the expression of β-Catenin protein in cells was analyzed by WB; and nuclear entry of β-Catenin was examined by Immunofluorescence. Results: Ginsenoside Rg3 inhibited the proliferation of SGC7901 cells in a time- and concentrationdependent manner; compared with the blank group, 40 mg/L Rg3 significantly inhibited the invasion and migration of SGC7901 cells (both P<0.05) and VM formation (P<0.05); in the meanwhile, the expressions of intracellular GSK-3β, Wnt2B mRNA and β-catenin protein, as well as the nuclear entry of β-catenin were significantly inhibited (all P<0.05). The invasion, migration and VM formation of SGC7901 cells in Rg3+BML-284 group were not significantly different from those in the blank group (all P>0.05). Conclusion: Rg3 can inhibit cell invasion, migration and VM formation in SGC7901 cells by inhibiting the activation of Wnt/β-Catenin pathway.