摘要
目的探讨化疗药物对肿瘤坏死因子相关细胞凋亡诱导配体(TRAIL)受体DR5在原代白血病细胞表达变化的作用。方法取10例急性白血病患者骨髓单个核细胞,分6组在体外培养:未处理组,阿克拉霉素(AcLa)处理组,足叶乙甙(VP-16)处理组,阿糖胞苷(Ara-c)处理组,AcLa+Ara-c处理组和VP-16+Ara-c处理组。培养72h后,用流式细胞仪检测DR5的表达。结果未处理组原代白血病细胞表达TRAIL-DR5的水平较低,平均荧光强度(MFI)为13±4,AcLa及AcLa+Ara-c上调TRAIL-DR5在原代白血病细胞的表达(MFI分别为41±14和47±15),而VP-16,Ara-c和VP-16+Ara-c对DR5的表达水平无明显影响。结论AcLa及AcLa+Ara-c在体外上调原代白血病细胞表达DR5水平,提示AcLa可能通过TRAIL凋亡途径诱导白血病细胞发生凋亡而发挥其抗白血病作用,而且与Ara-c联合应用有协同效应。
Objective To explore the effect of chemotherapeutic reagents on the expression of TRAIL receptor DR5 on primary acute leukemia cells. Methods Bone marrow mononuclear cells （BMMNC） from 10 cases of acute leukemia were cultured in vitro in 6 groups ： untreated, AcLa treatment, VP - 16 treatment, Ara - c treatment, AcLa ＋ Ara - c treatment, and VP - 16 ＋ Ara - c treatment. After cultured for 72h, the expression of DR5 was analyzed by flow cytometry. Results The expression of DR5 in untreated BMMNC from 10 cases of acute leukemia was low with MFI at 13 ±4. AcLa and AcLa ＋ Ara - c upregulated the expression of DR5 on BMMNC with MFI at 41 ±14 and 47 ± 15 ,respectively. However, the expression of DR5 on BMMNC was not modulated by the treatment of VP - 16 ,Ara - c and VP - 16 ＋ Ara - c. Conclusion AcLa and AcLa ＋ Ara - c upregulate the expression of DR5 on primary leukemia cells, suggesting that AcLa may exert its anti - leukemia effects by inducing leukemia cell apoptosis mediated by TRAIL induced apoptosis pathway. Ara - c augments the effects of AcLa.
出处
《中原医刊》
2006年第8期20-22,共3页
Central Plains Medical Journal
