EGCG通过下调Bcl-2诱导KG1A白血病细胞凋亡

EGCG-induced apoptosis in leukemia cells via down-regulation of Bcl-2

目的研究EGCG对KG1A白血病细胞的作用,探讨其作用机制。方法使用人的白血病细胞株KG1A细胞。MTT细胞毒性测定评价对白血病细胞的作用,使用annexin v染料标记细胞,应用流式细胞仪检测细胞凋亡。RT-PCR检测KG1A细胞Bcl-2家族mRNA的表达。结果EGCG引起KG1A细胞活性的下降。EGCG诱导KG1A细胞凋亡,且呈时间依赖性。EGCG诱导凋亡与下调Bcl-2和Bcl-xl有关。结论EGCG可以通过下调Bcl-2和BCl-xl诱导KG1A细胞凋亡。这些结果有助于提供新的有效联合方案,尤其是针对复发难治白血病的治疗。

Objective To investigate the effects and mechanism of EGCG on KG1A vayelold leukemia cell line. Methods Human rnyeloid leukemia cells KG1A were used. The cytotoxicity was analyzed by MTT assay. Apoptosis were detected by flow cytometry using annexin v dye. The expressions of Bcl - 2 family were detected by RT - PCR. Results EGCG resulted in decreased viability in KG1A cells. EGCG induces apoptosis in a time - dependent manner. EGCG - in- duced apoptosis was correlated with down - regulation of Bcl - 2 and Bcl - xl. Conclusion EGCG induces apoptosis in KG1A cells via down - regulation of Bel -2 and Bcl - xl. It is possible to design a better reagents for EGCG - based thera- peutic interventions against leukemia.