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为了研究重组变构人肿瘤坏死因子相关凋亡诱导配体(recombinanat mutant human TRAIL,rmhTRAIL)单用及与柔红霉素(DNR)联合应用对白血病细胞株U937、K562的诱导凋亡作用及其机制,以正常人胚肺成纤维细胞株MRC-5作对照,采用MTT法检测体外培养的U937、K562白血病细胞株在rmhTRAIL单用和联合DNR作用下增殖的抑制效应;用半定量逆转录多聚酶链反应(RT-PCR)法检测DNR处理前后白血病细胞TRAIL死亡受体和诱杀受体的mRNA表达水平。结果表明rmhTRAIL对白血病细胞株U937、K562有较明显的抑制增殖作用,DNR与TRAIL联合对抑制肿瘤细胞具有协同性,与各药单独使用比较均有显著差异(P<0.05);经DNR作用后,U937、K562细胞的死亡受体DR4、DR5水平上调,而两种诱杀受体DcR1、DcR2表达未受影响。结论在体外rm-hTRAIL单用或与DNR联用均能明显抑制白血病细胞增殖,rmhTRAIL与DNR对白血病细胞的杀伤有协同作用,其诱导机制可能与U937、K562细胞死亡受体DR4、DR5表达水平上调有关。
The aim of this study was to investigate the apoptosis-inducing effect of recombinanat mutant human TRAIL (rmhTRAIL) and its combination with daunorubicin (DNR) on leukemia cell lines U937 and K562 The normal human embryonic lung fibroblast cell line MRC-5 was used as a control. The inhibitory effects of rmhTRAIL alone and in combination with DNR on the proliferation of U937 and K562 leukemia cell lines were detected by MTT assay. Semiquantitative reverse transcription polymerase The mRNA expression levels of TRAIL death receptor and decoy receptor of leukemia cells before and after treatment with DNR were detected by reverse transcription-polymerase chain reaction (RT-PCR). The results showed that rmhTRAIL could significantly inhibit the proliferation of leukemia cell lines U937 and K562. The combination of DNR and TRAIL had synergistic effect on the inhibition of tumor cells, which was significantly different from that of each drug alone (P <0.05) , U937, K562 cell death receptors DR4, DR5 levels were upregulated, while the two decoy receptors DcR1, DcR2 expression was not affected. Conclusion Both rm-hTRAIL and DNR could inhibit the proliferation of leukemia cells in vitro. The mechanism of rmhTRAIL and DNR on killing leukemia cells is synergistic. The mechanism of rmhTRAIL may be related to the expression of DR4 and DR5 on U937 and K562 cell death receptors Up-related.