MAb225影响Tca8113细胞放射敏感性的机制探讨

目的：探讨表皮生长因子受体单抗调控Tca8113细胞放射敏感性的作用机制.方法：以不同浓度的MAb225处理Tca8113细胞,采用流式细胞术和双荧光染色分析法,观察细胞放射后凋亡的变化;以碱性单细胞凝胶电泳法检测细胞在放射后DNA损伤修复的变化,应用流式细胞法分析细胞周期的变化,分光光度法检测细胞内GSH水平的变化.结果：应用0.5μg/ml MAb225或6Gy放射处理Tca8113细胞,可使细胞的凋亡提高1倍左右,而联合应用可使凋亡比例上升至5～6倍（F检验）;MAb225处理的细胞放射后DNA损伤的修复慢于未处理组,两者的慧尾长度在放射后的30min内均有显著性差异（t检验,P＜0.05）;流式细胞分析显示,G1期细胞比例上升而S期细胞比例下降;MAb225处理的细胞,其GSH水平明显低于未处理的细胞,两者间有显著性差异（t检验,P＜0.05）.结论：MAb225影响细胞放射敏感性的机制与MAb225诱导放射后凋亡、抑制DNA修复、改变细胞周期再分配和影响GSH水平有关.

The mechanism of MAb225 regulating radiosensitivity of Tca8113 cell

PURPOSE: The objective of this study was to investigate the mechanism of MAb225 regulating radiosensitivity of Tca8113 cells. METHODS: Tca8113 cells were treated with MAb225 of different concentrations. The apoptosis rate was analysed by FCM and bi-fluorescence stain, the repair of DNA damage after radiation was analysed by single cell gel electrophoresis, cells redistribution in each phase of cell cycle was analysed by FCM, and GSH level of cell were assessed by spectrophotometer. RESULTS: Radiation alone (6 Gy) and MAb225 alone (0.5 microg/ml) produced a 2-fold induction of apoptosis respectively, whereas exposure to MAb225 (0.5 microg/ml) combination with 6 Gy of radiation induced apoptosis 5-6 fold, compared to untreated controls (F test). The length of comet tail of cells which treated with MAb225 was significantly longer than that of the control cells (t test, P<0.05). The percentage of cells in S phase was significantly decreased in MAb225 treated cells. Intracellular GSH level of MAb225 treated cells was significantly lower than that of untreated cells (t test, P<0.05). CONCLUSION: MAb225 increased the radiosensitivity of Tca8113 cells by enhancing radiation-induced apoptosis, downregulating S phase percentage, inhibiting DNA repair after radiation and decreasing GSH level.