黄芪甲苷通过Wnt/β-catenin途径影响HepG-2细胞的增殖和凋亡

Astragaloside Affects HepG-2 Cell Proliferation and Apoptosis Through Wnt/β-Catenin Pathway

目的:分析黄芪甲苷(Astragaloside IV,AS-IV)对HepG2细胞作用后产生的效应及其具体机制。方法:使用不同浓度AS-IV(25、50、100 nmoL/L)干预HepG2细胞,采用Trans-well法、细胞划痕实验和免疫荧光法分析HepG2细胞系的侵袭和迁移情况。Westeblot检测Caspase-3、Caspase-9、VEGF、MMP-14、E-cadherin、N-cadherin、Wnt、β-catenin和TCF-4等蛋白的表达的变化。结果:CCK-8法检测显示AS-IV刺激HepG2细胞时可抑制HepG2细胞的生长,促进细胞凋亡。细胞划痕实验以及Trans-well实验显示AS-IV能明显抑制HepG2细胞的侵袭和迁移。Western blotting检测显示AS-IV干预HepG2细胞后,VEGF和MMP-14蛋白水平、N-cadherin和vimentin的表达量降低(P<0.05),Caspase-3和Caspase-9表达量上升。同时,AS-IV还可抑制HepG2细胞的Wnt、β-catenin和TCF-4蛋白的表达。结论:黄芪甲苷通过调节Wnt/β-catenin途径影响HepG-2细胞的生物学过程。

Objective:To analyze the effect of Astragaloside IV(AS-IV)on HepG2 cells and its mechanism.Methods:HepG2 cells were intervened with different concentrations of AS-IV(25,50,100 nmol/L).The invasion and migration of HepG2 cells were analyzed by Trans-well,wound healing and immunofluorescence assay.Western blot was used to detect the expression of Caspase-3,Caspase-9,VEGF,MMP-14,E-cadherin,N-cadherin,Wnt,β-Catenin and TCF-4.Results:CCK-8 assay showed that AS-IV-could inhibit the growth of HepG2 cells and promote apoptosis.Wound healing and trans-well showed that AS-IV could significantly inhibit the invasion and migration of HepG2 cells.Western blotting showed that VEGF and MMP-14 protein levels,N-cadherin and vimentin expression decreased,Caspase-3 and Caspase-9 expression increased after AS-IV intervention in HepG2 cells(P<0.05).At the same time,AS-IV can inhibit the expression of Wnt,β-Catenin and TCF-4 protein in HepG2 cells.Conclusion:Astragaloside IV affects the biological process of HepG-2 cells by regulating Wnt/β-Catenin pathway.