目的 探讨荷包牡丹碱对人肝癌MHCC97-H细胞转移、侵袭的影响及潜在机制。方法 体外培养MHCC97-H细胞至对数生长期，分别经5、10、25、50、100 μmol/L荷包牡丹碱处理24、48、72 h，MTT法检测细胞增殖能力。5、10、25 μmol/L荷包牡丹碱处理MHCC97-H细胞24 h，MTT法检测细胞黏附能力，细胞划痕实验检测细胞转移能力，Transwell小室实验检测细胞侵袭能力，实时荧光定量PCR（qRT-PCR）实验检测VEGF、MMP-2及MMP-9基因表达水平，蛋白免疫印迹实验检测p-JAK2及p-STAT3蛋白表达水平。结果 25 μmol/L荷包牡丹碱处理MHCC97-H细胞48、72 h及50、100 μmol/L荷包牡丹碱处理24、48、72 h后的细胞活力下降明显，与对照组比较，差异显著（P<0.05、0.01）；5、10、25 μmol/L荷包牡丹碱处理MHCC97-H细胞24 h，细胞黏附能力、伤口愈合能力、穿膜数均明显下降（P<0.05、0.01），VEGF、MMP-2、MMP-9基因表达及p-JAK2、p-STAT3蛋白表达均明显下降（P<0.05、0.01）。结论 荷包牡丹碱可以抑制人肝癌MHCC97-H细胞的转移及侵袭，该作用与下调VEGF、MMP-2、MMP-9基因表达及抑制JAK2/STAT3信号通路的活化有关。

Objective To detect the effects of dicentrine on the migration and invasion of human hepatocellular carcinoma MHCC97-H cells and potential mechanisms. Methods MHCC97-H cells were cultured in vitro and cultured at logarithmic growth stage. The cells were treated with 5, 10, 25, 50, 100 μmol/L dicentrine for 24, 48, 72 h, and cell proliferation was determined by MTT assay. The cells were treated with 5, 10, 25 μmol/L dicentrine for 24 h, the cell adhesion, cell migration, cell invasion, gene expression of VEGF, MMP-2 and MMP-9, and protein expression of p-JAK2 and p-STAT3 were determined by MTT, scratch, Transwell, real-time qPCR, and western blot assay, respectively. Results The cell viability of MHCC-97H cells treated with 25 μmol/L dicentrine at 48 and 72 h, and 50 and 100 μmol/L dicentrine at 24, 48, and 72 h was decreased significantly, which was significantly different from that of the control group (P<0.05 or P<0.01). Compared with control group, cell adhesion ability, wound healing ability, cell penetration modulus, gene expression of VEGF, MMP-2 and MMP-9, and protein expression of p-JAK2 and p-STAT3 of MHCC-97H cells treated with 5, 10 and 25 μmol/L dicentrine at 24 h were decreased significantly (P<0.05 or P<0.01). Conclusion Dicentrine can inhibit the migration and invasion of human hepatocellular carcinoma MHCC97-H cells, which is related to the down-regulation of VEGF, MMP-2, and MMP-9 gene expression and inhibition of JAK2/STAT3 signaling pathway activation.