TRAIL与5-FU联合诱导白血病细胞凋亡的分子机理研究

用凋亡诱导配体（TRAIL）及5-氟尿嘧啶（5-FU）联合刺激Jurkat细胞36h，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 b-lotting）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。

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

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.