TRAIL与5-FU联合诱导白血病细胞凋亡的分子机理研究  

Synergistic effect of TRAIL and 5-FU on human leukamic Jurkat T cells

作　　者：程宏[1] 祝瑾[1] 贾筱琴[1] 

机构地区：[1]扬州大学医学院,江苏扬州225001

出　　处：《扬州大学学报（农业与生命科学版）》2005年第4期12-15,共4页Journal of Yangzhou University：Agricultural and Life Science Edition

基　　金：江苏省高校自然科学研究指导性计划(05KJD310266)扬州大学自然科学基金资助项目(PK0410191)

摘　　要：用凋亡诱导配体(TRAIL)及5-氟尿嘧啶(5-FU)联合刺激Jurkat细胞36 h,以诱导细胞凋亡;用流式细胞术和 MTS比色法检测细胞存活率,计算细胞凋亡率;用免疫印迹(Western blotting)检测p53的表达和胱天肽酶-3、胱天肽酶-8的变化。结果表明:5-FU能有效增加TRAIL诱导的Jurkat细胞凋亡．并伴随p53表达增加及胱天肽酶-3和胱天肽酶-8的活性增加,提示TRAIL和5-FU联合诱导的T淋巴白血病细胞凋亡的分子机制与p53及胱天肽酶-3、胱天肽酶-8有关,为TRAIL和5-FU联合用于治疗白血病提供理论依据。To investigate the signal pathway and expression of related proteins in apoptosis of T lymphocyte （leukemia） induced by TRAIL and 5-FU, providing a novel insight and information in the apoptosis signaling pathways induced by TRAIL and chemical reagents and providing an important implication for the clinic therapy of T-lymphocyte leukemia. Jurkat cells treated with TRAIL and 5-FU for 36 h were used to detect the viability with MTS assay and flow cytometry, and to detect caspase-8, caspase-3 and p53 expression with western blot. The results showed that 5-FU could increase the apoptotic rate of Jurkat cells induced by TRAIL with activation of caspase-8, caspase-3 and enhancement of p53 expression. It was illuminated for the first time that the molecular mechanism and signal pathways of apoptosis of T-lymphocyte leukemia induced by TRAIL and 5-FU might involve caspase-8, caspase-3 and p53.

关 键 词：白血病 凋亡诱导配体 5-氟尿嘧啶 细胞凋亡 免疫印迹 

分 类 号：R733.7[医药卫生—肿瘤]