探讨新型光敏剂ZnPcH1介导的光动力疗法对K562细胞的杀伤效应及其杀伤机制。应用MTT比色法检测光动力疗法对K562细胞增殖能力的影响; 采用AO/EB荧光染色法、DNA片段化分析、TUNNEL、Annexin-V-FITC/PI双染法等检测ZnPcH1-PDT诱导K562细胞的死亡方式; 以RT-PCR法检测ZnPcH1-PDT作用后不同时间对K562细胞c-myc、人端粒酶逆转录酶蛋白催化亚单位(htert)、survivin、caspase-3 mRNA表达的变化。研究发现MTT比色法结果显示PDT可以抑制K562细胞的增殖, 抑制率随光敏剂浓度的增加而增高; 各凋亡检测结果均显示ZnPcH1-PDT可诱导K562细胞凋亡, 且呈时间依赖性; ZnPcH1-PDT处理K562细胞后c-myc、htert、survivin mRNA表达呈时间依赖性降低, 而caspase-3 mRNA表达呈时间依赖性增强。结果提示PDT能抑制K562细胞增殖, 诱导细胞凋亡。

The present research is to investigate the effect of ZnPcH1-based-photodynamic therapy (ZnPcH1-PDT )on K562 cells and the possible mechanisms.The survival rate of cells was assessed by MTT method. The cell death patterns was assessed by AO/EB stain,DNA fragmentation assay,TUNEL method and Annexin-V-FITC/PI double stains.The levels of c-myc,htert, survivin and caspase-3 mRNA were decided by reverse transcriptase polymerase chain reaction(RT-PCR) in the post-PDT cells.The result of MTT method showed that PDT presented anti-proliferation effect on K562 cells.Furthermore,the results of apoptosis detection all revealed that PDT could induce K562 cells apoptosis in a time-dependent manner.The expression of c-myc, htert and survivin were significantly down- regulated (P<0.05),while the levels of caspase-3 mRNA were significantly up-regulated (P<0.05) in the post-PDT cells.The research indicated that ZnPcH1-PDT have anti-proliferation effect and could induce K562 cells apoptosis.