摘要
目的探究硼替佐米对霍奇金淋巴瘤细胞系L428凋亡的影响及可能的机制。方法不同浓度的硼替佐米(0、10、30与50 nmol/L)培养L428细胞后,用倒置显微镜观察L428细胞形态;Hoechst33258染核观察细胞核;MTT法检测细胞活力;TUNEL染色试剂盒和Annexin V-FITC双染细胞凋亡试剂盒检测细胞凋亡;Western blot法检测凋亡相关蛋白cleaved caspase-3、Bax和Bcl-2的表达。结果与对照组相比,硼替佐米促使L428细胞出现拉丝、稀疏现象;细胞核出现核固缩和凋亡小体;硼替佐米浓度依赖性抑制L428细胞活力(P<0.05),诱导细胞凋亡(P<0.05);浓度依赖性下调Bcl-2蛋白水平(P<0.05);浓度依赖性上调cleaved caspase-3和Bax蛋白水平(P<0.05)。结论硼替佐米可能通过影响凋亡蛋白的表达促进霍奇金淋巴瘤细胞系L428凋亡。
Objective To investigate the effect of Bortezomib on Hodgkin lymphoma cell line L428 apoptosis. Methods L428 cells were treated with different concentrations of Bortezomib （0, 10, 30 or 50 nmol/L ）. Cell morphology was observed by inverted microscopy; nuclear morphology was determined by Hoechst33258 staining; cell viability was analyzed by MTT assay; cell apoptosis was measured by Annexin V-FITC double staining and TUNEL staining; the protein expression of cleaved caspase-3, Bax and Bcl-2 were detected by Western blot. Results Compared with control group, Bortezomib induced L428 cell appeard cliques, wire drawing, apoptsis body. Bortezomib concentration-dependently inhibited cell viability（ P 〈0.05）, increased cell apoptosis（ P 〈0.05）. Moreover, Bortezomib concentration-dependently caused up-regulation of the protein expressions of cleaved caspase-3 and Bax（ P 〈0.05）, but down-regulation of the protein expression of Bcl-2（ P 〈0.05）. Conclusions Bortezomib may increase L428 cell apoptosis through influencing the expression of apoptosis proteins.
作者
陈宛丽
关红梅
王舒
CHEN Wan-li;GUAN Hong-mei;WANG Shu(Dept.of Hematology,Nanyang Second General Hospital,Nanyang 473000,China)
出处
《基础医学与临床》
CSCD
2018年第10期1438-1442,共5页
Basic and Clinical Medicine
