Raji细胞抵抗阿霉素诱导细胞凋亡分子机制的实验研究  

MOLECULAR MECHANISM OF RESISTANCE APOPTOSIS ON HUMAN B LYMPHOMA RAJI CELLS INDUCED ADR

作　　者：田方[1] 李春海[1] 颜春洪[1] 程国均 陈高明[1] 

机构地区：[1]军事医学科学院附属医院,北京100039

出　　处：《白血病》2000年第4期206-209,共4页

摘　　要：目的 :观察 Raji细胞抵抗阿霉素诱导细胞凋亡的分子机制 ,从细胞凋亡的角度探讨肿瘤细胞耐药机制。方法 :MTT方法测定阿霉素和肽素诱导的细胞毒实验 ,碘化丙啶染色 FACS和 DNA降解断裂法分析阿霉素诱导的细胞凋亡 ,FACS分析 Raji细胞 bcl- 2的表达 ,Western bolt观察 Raji细胞 p5 3、bax分子的表达 ,RT- PCR检测 MDR1、MRP和 GSTπ的表达水平。结果 :Raji细胞对阿霉素和肽素均产生明显药物耐受 ,同时抵抗药物诱导的细胞凋亡 ;Raji细胞中 bcl- 2分子呈诱导性表达 ,不表达或弱表达 bax、p5 3分子 ;Raji细胞组成性高表达 MDR1、MRP、GSTπ等耐药相关分子。结论 :Raji细胞抵抗药物诱导的细胞凋亡是化疗耐受的重要原因。其中细胞膜表面分子 MDR1、MRP的高表达 ,细胞质中 bcl- 2诱导性高表达 ,bax、p5 3分子的弱表达是导致药物耐受和抵抗细胞凋亡的重要因素。Objective:To explore the molecular mechanism of resistance apoptosis on human B lymphoma Raji cell induced Adr.Methods:MTT assays analysis induced Adr cytotoxicities in Raji cells and U937.Apoptosis was judged by the appearance of specific DNA ladders on agarose gel electrophoresis.Flow cytomeyic analysis for bcl 2 expression.Immunoblotting for bax.p53.RT PCR analysis for MDR1,MRP and GSTπ expression.Results:Raji cells were resistant to Adr and Tax treatment and their survival rates was not suppressed by Tax.Induction of DNA fragmentation in Tax sensitive U937 cells,but not in Tax resisitance Raji cells.U937 cells expressed bcl 2 protein,and the Expression of bcl 2 was even less in Raji cells.Raji cells also did not express a detectable level of bax and p53 proteins.Conclusion:Raji cells have been found to resistance apoptosis that induced by Adr,this is close associated with theirs drug resistance.bcl 2,bax and p53 are important of drug induced apoptosis thereby modulating resistance to chemotherapy.

关 键 词：RAJI细胞 药物耐受 细胞凋亡 肿瘤 

分 类 号：R730.2[医药卫生—肿瘤]