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目的探讨表没食子儿茶素没食子酸酯(EGCG)对肝癌HepG2细胞增殖和侵袭的影响及可能的分子机制。方法不同浓度EGCG对HepG2细胞进行干预后,CCK-8法检测EGCG对肝癌HepG2细胞增殖的影响;荧光显微镜及流式细胞术(FCM)Annexin V-FITC/PI双染法检测EGCG对HepG2细胞的凋亡诱导作用;Transwell侵袭实验检测EGCG对HepG2细胞侵袭的影响;ELISA法检测HepG2细胞中基质金属蛋白酶-2(MMP-2)和血管内皮生长因子(VEGF)的表达水平。结果EGCG各浓度组干预HepG2细胞24、48h后,细胞的生长增殖均明显受到抑制,其24h IC25值和IC50值分别为58.19和133.90mg/L。以60、135mg/L EGCG干预肝癌HepG2细胞24h后,FCM结果显示药物组细胞凋亡率明显高于对照组(P<0.05),荧光显微镜观察显示随着药物浓度的增加,细胞凋亡程度加重。Transwell侵袭实验显示,60、135mg/L EGCG对HepG2细胞侵袭力抑制率分别为69.47%和100%(P<0.05)。ELISA检测结果显示,EGCG干预后HepG2细胞上清液中MMP-2和VEGF表达水平下降(P<0.05)。结论 EGCG对人肝癌HepG2细胞具有抑制增殖和侵袭作用,其机制可能与EGCG诱导HepG2细胞凋亡和抑制肿瘤细胞中MMP-2及VEGF表达水平有关。
Objective To investigate the effects of epigallocatechin-3-gallate (EGCG) on the proliferation and invasion of HepG2 hepatocarcinoma cells and the possible molecular mechanisms. Methods The effects of EGCG on the proliferation of HepG2 cells were detected by CCK-8 assay with different concentrations of EGCG on HepG2 cells. The proliferation of HepG2 cells was detected by fluorescence microscope and flow cytometry (FCM) Annexin V-FITC / PI double staining The effect of EGCG on the invasion of HepG2 cells was detected by Transwell invasion assay. The expression of matrix metalloproteinase-2 (MMP-2) and vascular endothelial growth factor (VEGF) in HepG2 cells was detected by ELISA. Results After 24h and 48h treatment of HepG2 cells, the growth and proliferation of HepG2 cells were significantly inhibited by EGCG. The 24h IC25 and IC50 values of EGCG were 58.19 and 133.90 mg / L, respectively. FCM results showed that the apoptosis rate of HepG2 cells treated with EGCG at 60 and 135 mg / L for 24 h was significantly higher than that of the control group (P <0.05). Fluorescence microscopy showed that the apoptosis rate was increased with the increase of drug concentration . Transwell invasion assay showed that the inhibitory rates of invasion of HepG2 cells by 60 and 135 mg / L EGCG were 69.47% and 100%, respectively (P <0.05). The results of ELISA showed that the expression of MMP-2 and VEGF in HepG2 supernatant decreased after EGCG treatment (P <0.05). Conclusion EGCG can inhibit the proliferation and invasion of human HepG2 cells. The possible mechanism is that EGCG may induce the apoptosis of HepG2 cells and inhibit the expression of MMP-2 and VEGF in tumor cells.