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目的研究热化疗对肺部肿瘤细胞生长影响的可能机制。方法参考临床常用剂量,采用43℃加热联合50μg/L紫杉醇(热化联合组)、单纯使用50μg/L紫杉醇(单纯化疗组)处理A549细胞,以未处理的A549细胞作对照,应用噻唑蓝比色法(MTT法)检测各处理方式下细胞增殖率,荧光法检测细胞内活性氧(ROS),按LDHKit要求检测LDH活力,SPSS 13.0对数据进行统计分析。结果热化联合组细胞增殖率(56.34±4.30)%低于对照组和单纯化疗组(P<0.05);ROS在热化联合组增高(139.93±37.59)(P<0.05),热化联合组D的LDH(3732.76±172.99)较对照组(68847.25±559.32)和单纯化疗组(14771.65±417.13)明显减少(P<0.05)。结论热化疗联合应用可以明显抑制A549细胞的生长,这种抑制作用可能是通过诱导ROS的产生,损伤肺肿瘤细胞膜实现的。
Objective To study the possible mechanism of thermochemotherapy on the growth of lung tumor cells. Methods With reference to the commonly used clinical dose, A549 cells were treated with combination of 50μg / L paclitaxel (heating combined with heat treatment at 43 ℃) and paclitaxel (chemotherapy alone) at 50μg / L, untreated A549 cells were treated with thiazolyl blue MTT assay was used to detect cell proliferation rate. Fluorescence was used to detect intracellular reactive oxygen species (ROS). LDHKit was used to detect LDH activity. SPSS 13.0 was used to analyze the data. Results Compared with the control group and chemotherapy alone group (56.34 ± 4.30)%, the proliferation rate of the combined therapy group was significantly lower (P <0.05). The ROS level in the combination group was higher (139.93 ± 37.59) (P <0.05) Compared with the control group (68847.25 ± 559.32) and chemotherapy alone group (14771.65 ± 417.13), the LDH of D group (3732.76 ± 172.99) was significantly decreased (P <0.05). Conclusion The combination of hyperthermia and chemotherapy can significantly inhibit the growth of A549 cells, and this inhibition may be through the induction of ROS generation, damage lung cell membrane to achieve.