表没食子儿茶素没食子酸酯对人膀胱癌T24细胞凋亡的影响

Effects of EGCG on apoptosis of human bladder carcinoma T24 cells

目的研究表没食子儿茶素没食子酸酯(EGCG)在体外对人膀胱癌细胞系T24细胞凋亡的诱导作用,并探讨其诱导凋亡的相关信号通路等分子机制。方法应用光学显微镜和流式细胞仪检测EGCG作用T24细胞的凋亡诱导作用。采用Western blotting方法检测PI3K/Akt信号通路的改变;同时研究了caspase-3,PARP等蛋白在诱导细胞凋亡中的作用。结果EGCG作用于T24细胞24h后能明显诱导细胞凋亡,呈显著浓度依赖性。EGCG使T24细胞caspase-3和PARP均被激活;T24细胞phospho-Thr308-Akt和phospho-Ser473-Akt的表达逐渐降低,但t-Akt未见改变。结论EGCG能诱导T24细胞凋亡,EGCG凋亡诱导作用可能和抑制PI3K/Akt信号通路的激活有关。

Objective To study the effects of EGCG on apoptosis of T124 cells in vitro and to identify the relative signaling pathway（s）. Methods The induction of apoptosis by EGCG was measured by analyzing cell morphology and by PI staining and the annexin V method. Alterations of activating （phospho - ） PI3K/Akt pathway were determined by Western blot. The roles of caspase 3 and PARP in induction of apoptosis were analyzed at the same time. Results EGCG could induce significant apoptosis in dose-dependent manner after T24 cells had been treated with ECCC for 24 hours. EGCG could lead to activation of caspase-3 and PARP proteins and down-regulation of protein expression of phospho-Thr308-Akt and phospho-Ser473-Akt without any effect on total Akt expression in T24 cells. Conclusion EGCG can induce apoptosis of T24 cells which may be induced by the way of prohibiting activating （phospho-） PI3K/Akt pathway.