论文部分内容阅读
鬼臼噻吩甙(VM-26)能抑制拓扑异构酶(Top Ⅱ)使DNA单、双链可逆性断裂,并能使细胞阻滞于S后期和G_2+M期。通过克隆形成法探讨VM-26与放射联合应用对人肺腺癌细胞(SPC)的影响,发现二者能取得协同作用。剂量修饰因子为1.47(0.125μM作用1h,生存率为0.01水平)。从细胞存活曲线看,平均致死剂量Do变化不大(1.46Gy对1.40Gy),但用药后照射肩区消失,说明VM-26能抑制SPC细胞亚致死性损伤修复,但不改变细胞放射敏感性。放射前或后给药细胞存活率差异无显著性。
Peptidomimetic (VM-26) inhibits topoisomerase (Top II) to reversibly disrupt single and double stranded DNA, and arrest cells in the late S phase and G2 + M phase. The effect of combined application of VM-26 and radiation on human lung adenocarcinoma cells (SPC) was investigated by colony formation assay and it was found that the two could achieve synergistic effects. The dose modification factor was 1.47 (0.125 μM effect for 1 h, survival rate 0.01 level). From the cell survival curve, the average lethal dose Do did not change much (1.46 Gy vs. 1.40 Gy), but the irradiated shoulder area disappeared after treatment, indicating that VM-26 can inhibit the sub-lethal damage repair of SPC cells, but does not change the cellular radiosensitivity . There was no significant difference in cell viability before or after radiation.