中文摘要：

目的：探讨在体外恶性淋巴瘤细胞对TRAIL（TNF—related apoptosis—inducing ligand）诱导凋亡的抵抗作用及其分子机制。方法：TRAIL处理恶性淋巴瘤U937细胞后，在不同的时间采用MTT法检测药物对细胞的毒性作用；流式细胞术检测细胞周期；Western—blot法检测Bax蛋白质水平变化；实时荧光定量RT—PCR法检测BaxmRNA的表达情况。结果：TRAIL的浓度在500μg／L时可抑制U937的细胞生存，但其抑制率低于正常对照细胞Hmy2．ciR；TRAIL阻滞U937细胞周期于G0／G，期；但这种阻滞效应较Hmy2．ciR细胞明显减弱。Western—blot法检测TRAIL处理的U937细胞Bax蛋白表达水平下降；实时荧光定量RT—PCR法检测BaxmRNA的表达水平却未见差异性改变。结论：TRAIL在诱导恶性淋巴瘤细胞凋亡过程中出现抵抗，这种作用可能与促凋亡蛋白Bax表达水平下降有关。Bax蛋白表达水平的下降可能是由于翻译后修饰导致Bax蛋白降解。

英文摘要：

Objective： To investigate the mechanism of TRAIL-induced apoptotic resistance in lymphoma cells. Methods： U937 cells were treated with TRAIL in vitro and the cell growth index was evaluated by MTT assay. The cell cycle was detected by flow cytometry. The levels of Bax protein and mRNA were measured by Western blot and real time RT-PCR, respectively. Results： TRAIL inhibited survival of U937 cells at a concentration of 500 μg/L, but the inhibition rate was lower than that in the control cells （Hmy2.ciR）. TRAIL arrested U937cells in G0/G1 phases, but this effect was significantly weaker when compared to that in the control cells. Further studies showed that the Bax protein level was decreased in TRAIL-treated U937 cells but no change was found in Bax mRNA expression. Conclusion： U937 cells are resistant to TRAIL-induced apopto- sis. This effect may be related to a decrease in Bax protein which may be caused by degradation of Bax at the post-translational level in TRAIL-treated U937 cells.