大蒜素对人子宫内膜癌Ishikawa细胞侵袭和迁移抑制作用的研究

Inhibition of allicin on invasion and migration of human endometrial cancer ishikawa cells

目的:探索大蒜素对人子宫内膜癌Ishikawa细胞侵袭和迁移的抑制作用及其调控机制。方法:取对数生长期人子宫内膜癌Ishikawa细胞为受试细胞,设空白对照组(DMSO),大蒜素低、中、高剂量组(12.5、25、50μg/ml)和顺铂组(40μg/ml)。药物干预48 h后,CCK-8法检测细胞增殖抑制率,PI染色流式细胞术分析细胞周期分布,Transwell小室法、划痕实验检测细胞侵袭能力和迁移能力,Western blot法检测MMP-2、MMP-9、E-cadherin、PI3K、p-Akt蛋白表达。结果:经大蒜素中、高剂量或顺铂干预能够明显提高Ishikawa细胞增殖抑制率,提高处于G0/G1期Ishikawa细胞比例,降低Ishikawa细胞侵袭能力和迁移能力,下调MMP-2、MMP-9、E-cadherin、PI3K、p-Akt蛋白表达量,较空白对照组比较,差异均具有统计学意义(P<0.05)。结论:大蒜素对人子宫内膜癌Ishikawa细胞侵袭和迁移具有明显抑制作用,其机制可能与阻滞细胞周期进程而抑制细胞增殖,降低MMP-2、MMP-9、E-cadherin蛋白表达以及抑制PI3K/Akt通路活性有关。

Objective:To investigate the inhibition effects of allicin on invasion and migration of human endometrial cancer Ishikawa cells and its mechanism.Methods:Take human endometrial cancer Ishikawa cells in logarithmic growth phase as test cells;set blank control group(DMSO),allicin low,medium and high-dose group(12.5,25,50μg/ml),and cisplatin 40μg/ml group.48 h after the drugs were given,the Ishikawa cells proliferation inhibition rate was detected by CCK-8 method;the cell cycle distribution was detected by flow cytometry;the ability of cell invasion was tested by transwell method;the ability of cell migration was measured by scratch test;the expression of MMP-2,MMP-9,E-cadherin,PI3K,p-Akt proteins were detected by western blot.Results:Intervented by medium,high-dose of allicin or intervented by cisplatin could increase Ishikawa cells proliferation inhibition rate,increase the percentage of Ishikawa cells in G0/G1 phase,decrease the Ishikawa cells'ability of invasion and migration,down-regulate the expression of MMP-2,MMP-9,E-cadherin,PI3K,p-Akt proteins,all of the difference compared with blank control group were significant(P<0.05).Conclusions:Allicin can inhibit the invasion and migration of human endometrial cancer Ishikawa cells;which mechanism may be related to blocking the cell cycle process to inhibit cell proliferation,down-regulate the expression of MMP-2,MMP-9,E-cadherin proteins and inhibit the activity of PI3K/Akt pathway.