硼替佐米对淋巴瘤细胞系CA46的作用及机制研究

Effect of Bortezomib on Lymphoma Cell Line CA46 and Its Relative Mechanisms

本研究探讨硼替佐米(bortezomib,BZM)对淋巴瘤细胞系CA46的作用及相关机制。采用MTT法观察BZM对CA46细胞增殖的作用,流式细胞术分析BZM对CA46细胞凋亡的影响,Western blot法检测经BZM作用的CA46细胞procaspase-3、BCL-2蛋白表达水平。结果表明,BZM能明显抑制CA46细胞增殖,24小时和48小时的半数抑制浓度(IC50)分别为53.19,19.68nmol/L;BZM能诱导CA46细胞凋亡,且呈现剂量和时间依赖性;20nmol/LBZM处理CA46细胞不同时间后procaspase-3、BCL-2蛋白表达呈时间依赖性降低。结论:BZM可以抑制CA46细胞增殖,诱导其凋亡,其机制可能涉及了BCL-2表达下调及caspase-3的活化。

The objective of this study was to explore the effect of bortezomib （BZM） on lymphoma cell line CA46 and its relative mechanisms in vitro. The effects of BZM on the proliferation and apoptosis of CA46 cells were assayed by MTT method and flow cytometry respectively. The effect of BZM on the expression levels of procaspase-3 and BCL- 2 protein were detected by Western blot. The results indicated that the BZM could inhibit the growth of CA46 cells significantly and the concentration of 50% growth inhibition （ ICs0 ） at 24 and 48 hours were 53.19 and 19.68 nmol/L respectively. After treatment with 20,40,80 nmol/L BZM for 24, 48 and 72 hours, a dose- and time-dependent apoptosis of CA46 cells could be observed. After treatment with 20 nmol/L BZM at different time point, a time-dependent reduction of procaspase-3 and BCL-2 protein expression in CA46 cells was found. It is concluded that the BZM can inhibit the proliferation and induce the apoptosis of CA46 cells, which relative mechanism may involve the reduction of BCL-2 and the activation of caspase 3.