【摘要】 本研究探讨8-溴-7-甲氧基白杨素(8-bromo-7-methoxyhysin,BrMChR)对人髓系白血病细胞株K562细胞增殖和凋亡的影响及细胞凋亡过程中caspase-3活性与p-Akt蛋白表达的变化。采用MTT方法检测BrMChR对K562细胞生长抑制的影响,用细胞形态学观察和流式细胞术分析细胞凋亡,Western blot方法检测p-Akt蛋白的表达。结果显示:与同浓度的白杨素(chrysin,ChR)相比,BrMChR对K562细胞的生长抑制作用及凋亡诱导作用更强,并随药物剂量的增加而加强;3μmol/L BrMChR作用K562细胞12小时细胞凋亡率可达21.8%,而同浓度的ChR作用K562细胞12小时细胞凋亡率仅为3.68%。随着BrMChR浓度增加,caspase-3活性增加(p<0.05),p-Akt蛋白表达下调(p<0.01)。结论 :BrMChR能诱导K562细胞凋亡,其作用强于ChR;p-Akt可能参与了BrMChR诱导K562细胞凋亡过程。更多还原

【Abstract】 This study was purposed to investigate the apoptosis-inducing effect of 8-bromo-7-methoxyhysin(BrMChR) on leukemia K562 cells as well as the variation of caspase-3 activity and phosphorylated Akt(p-Akt) expression of K562 cells during the process of apoptosis.MTT assay was used to determine the inhibitory effect of BrMChR on proliferation of K562 cells.Cell apoptosis was assayed by AO/EB staining under fluorescent microscope and flow cytometry with Annexin V-FITC/PI staining.The expression level of p-Akt was measured by Western blot.The results showed that BrMChR had the inhibitory effect on proliferation of K562 cells and could induce apoptosis of these cells in dose-dependent manner,and these effects were significantly stronger than ChR.After treatment of K562 cells with 3 μmol/L ChR for 12 hours,the apoptosis rate was only 3.68%,but the apoptosis rate of K562 cells treated with 3 μmol/L BrMChR was 21.8%.In the same time,the caspase-3 activity significantly increased(p<0.05),but the expression of p-Akt was down-regulated(p<0.01).It is concluded that BrMChR can induce apoptosis of K562 cells and with effect stronger than chR.P-Akt may participate in the apoptosis process of K562 cells induced by BrMChR.更多还原