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[目的]研究亚毒性浓度阿霉素联合TRAIL蛋白对肝癌HepG2细胞增殖及TRAIL受体表达的影响。[方法]采用MTT法,分别检测阿霉素、TRAIL及亚毒性浓度阿霉素联合TRAIL对HepG2细胞的生长抑制率;RT-PCR和Westernblot分别检测阿霉素作用前后HepG2细胞TRAIL受体DR4、DR5、DcR1、DcR2mRNA和蛋白表达的水平。[结果]TRAIL对HepG2细胞增殖的抑制不存在浓度依赖性;阿霉素对HepG2细胞增殖的抑制作用存在浓度依赖性;亚毒性浓度阿霉素与亚毒性浓度TRAIL联用杀伤肿瘤的能力明显增强;无论在mRNA还是蛋白水平,阿霉素处理后HepG2细胞死亡受体DR4、DR5的表达水平显著增加,而阿霉素处理后诱骗受体DcR1、DcR2的表达量较阿霉素处理前明显减少。[结论]亚毒性浓度的阿霉素与亚毒性浓度的TRAIL联合应用具有协同作用,其机制可能是由于阿霉素在某种程度上增加了细胞表面死亡受体的表达,从而诱导了细胞凋亡的增加,说明TRAIL在肿瘤治疗方面存在潜在的应用价值。
[Objective] To investigate the effect of sub-toxic concentration of doxorubicin and TRAIL on the proliferation and TRAIL receptor expression of HepG2 cells. [Methods] The inhibitory rates of doxorubicin, TRAIL and TRAIL on the growth of HepG2 cells were detected by MTT assay. The expressions of DR4, TR4R, TRAIL and TRAIL in HepG2 cells were detected by RT-PCR and Western blot respectively. DR5, DcR1, DcR2 mRNA and protein expression levels. [Results] There was no concentration-dependent inhibition of TRAIL on HepG2 cell proliferation; the inhibitory effect of doxorubicin on HepG2 cell proliferation was concentration-dependent; the ability of sub-toxic concentration of doxorubicin combined with sub-toxic TRAIL to kill tumor was significantly enhanced ; At mRNA or protein level, the expression levels of DR4 and DR5, the death receptors of HepG2 cells, significantly increased after doxorubicin treatment, whereas the expression levels of DcR1 and DcR2 were significantly decreased compared with that before adriamycin treatment . [Conclusion] The combination of sub-toxic doxorubicin and sub-toxic concentrations of TRAIL has a synergistic effect. The possible mechanism is that doxorubicin increases the expression of cell surface death receptors to a certain extent and induces cell apoptosis Increased death, indicating that TRAIL in the treatment of cancer there is potential value.