论文部分内容阅读
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 investigated the possible molecular mechanism of epigallocatechin gallate (EGCG) -induced NB4 cell apoptosis. NB4 cells were treated with different concentrations of EGCG or NB4 cells were pre-treated with p38α inhibitor PD169316 and treated with EGCG. Cell proliferation was detected by CCK-8 (cell counting kit-8) method. Cell apoptosis was detected by FITC-Annexin V / PI double staining and protein expression of p38α, P-p38α, Bcl-2 and Bax Level. The results showed that with the increase of EGCG concentration, the proliferation rate of NB4 cells gradually decreased, and the apoptosis rate was significantly increased. The protein expression of P-p38α and Bax increased, which was positively correlated with the concentration of EGCG, while the protein level of Bcl-2 decreased. After treated with p38α inhibitor, the proliferation rate of NB4 cells was increased, the apoptosis rate was decreased, the protein expression of Bax was decreased, but the expression of Bcl-2 protein was not changed. The above results indicate that EGCG may induce apoptosis of NB4 cells in acute promyelocytic leukemia by activating p38α.