表没食子儿茶素没食子酸酯通过活化p38α诱导急性早幼粒细胞白血病NB4细胞凋亡  

Epigallocatechin Gallate Induces Acute Promyelocytic Leukemia NB4 Cells Apoptosis by Activation of p38α

作　　者：淦柳根 刘北忠[1,2] 单志灵 肖春兰[1,2] 徐婷[1,2] 宋浩[1,2] 李浏[2] 杨蓉[2] 钟梁[2] 

机构地区：[1]重庆医科大学附属永川医院,中心实验室,重庆402160 [2]重庆医科大学,临床检验诊断学教育部重点实验室,重庆市重点实验室,重庆400016

出　　处：《中国细胞生物学学报》2016年第7期770-776,共7页Chinese Journal of Cell Biology

基　　金：国家自然科学基金面上项目(批准号:81171658);重庆市自然科学基金计划重点项目(批准号:2011BA5037)资助的课题~~

摘　　要：该文研究了表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)诱导NB4细胞凋亡的可能分子机制。不同浓度梯度EGCG处理NB4细胞,或预先用p38α抑制剂PD169316处理NB4细胞,再用EGCG处理。用CCK-8(cell counting kit-8)方法检测细胞增殖情况,用FITC-Annexin V/PI双染色法检测细胞凋亡情况,用Western blot检测p38α、P-p38α、Bcl-2和Bax蛋白质表达水平。结果显示,随着EGCG浓度的升高,NB4细胞增殖率逐渐降低,细胞凋亡率明显升高。P-p38α和Bax蛋白质表达水平升高,与EGCG浓度呈正相关;而Bcl-2蛋白质表达水平降低。p38α抑制剂处理后,NB4细胞增殖率升高,凋亡率降低,Bax蛋白质表达水平降低,而Bcl-2蛋白质表达水平无明显变化。以上结果表明,EGCG可能通过活化p38α诱导急性早幼粒细胞白血病NB4细胞凋亡。This study was aimed to investigate the molecular mechanism of NB4 cells apoptosis induced by epigallocatechin gallate （EGCG）. NB4 cells were treated with EGCG in a dose-dependent manner. Or NB4 cells were pretreated with PD 169316, an inhibitor of p38α, then treated with EGCG. The proliferation of NB4 cells was detected by cell counting kit-8 （CCK-8） assay. The apoptosis of NB4 cells was measured by FITC-AnnexinV/ PI. The protein levels of p38α, P-p38α, Bcl-2 and Bax were detected by Western blot. The results indicated that EGCG treatment significantly inhibited the viability of NB4 cells in a dose-dependent manner. In addition, EGCG treatment induced apoptosis, increased Bax and P-p38α protein expression levels and decreased Bcl-2 protein expression levels. Pretreatment with PD169316 partially increased the viability of NB4 cells, meanwhile, blocked EGCG-induced apoptosis and inhibited EGCG-mediated increases in Bax expression, but not affected Bcl-2 expression. These results suggested that EGCG induced apoptosis in NB4 cells may through the activation of p38α.

关 键 词：EGCG NB4细胞 凋亡 p38α 

分 类 号：R285[医药卫生—中药学]