摘要
目的研究化疗药物诱导Raji恶性淋巴瘤细胞核因子-kB(NF-kB)活化与凋亡关系,并探讨地塞米松(DXM)对其的影响作用。方法采用电泳迁移率变动分析(EMSA)检测细胞NF-kB活化水平;采用TdT介导的dUTP缺口末端标记技术(Tuned)检测细胞凋亡。结果化疗药物诱导Raji恶性淋巴瘤细胞NF-kB活化与化疗药物诱导细胞凋亡明显相关,lμmol/LDXM能显著抑制阿糖胞苷(Ara-C)lμmol/L或鬼臼乙叉甙(VP-16)lμmol/L诱导的Raji细胞NF-kB活化,抑制率分别为48.68%和44.39%,并增强它们诱导Raji细胞凋亡的作用,凋亡增加率分别为57.8%和37.5%。Raji细胞在接触化疗药物前,NF-kB亦有一定程度的活化。结论化疗药物在诱导Raji恶性淋巴瘤细胞凋亡的同时活化NF-kB,DXM可通过抑制NF-kB活化以增强化疗药物诱导恶性淋巴瘤细胞凋亡的作用。
Objective To analyze the relationship between activation of nuclear factor-kB（NF-kB） and apoptosis of malignant lymphomnatous cells induced by chemotherapeutic drugs and to explore the influence of dexamethasone （DXM）. Methods Electrophoretic mobility shift assay （EMSA） was used to detect the activation of NF-kB,TUNEL was adopted to observe apoptosis induced by homoharringtonine （Ara-C） and etopside （VP-16） in Raji malignant lymphomnatous cells. Results The activation of NF-kB induced by Ara-C and VP-16 （1μmol/L）. Before exposed to chemotherapeutic agents, the activity of NF- κB could be found in Raji cells. Conclusion Chemotherapeutic drugs induce apoptosis, and activation of NF - κB of Raji cells. DXM enhances on apoptosis malignant lymphomnatous cells induced by chemotherapeutic drugs which may be related to suppression of the activation of NF - κB
出处
《医药论坛杂志》
2009年第22期3-6,共4页
Journal of Medical Forum
