中文摘要：

目的：研究热化疗抑制肺肿瘤细胞生长的可能机制及活性氧（ROS）在其中的作用。方法：采用6种不同热化疗联合方法处理H446细胞,以未处理的H446细胞作对照,用荧光法检测细胞内活性氧,蛋白免疫印记法检测JNK和Akt磷酸化水平,流式细胞术检测细胞凋亡率,SPSS13.0对数据进行统计分析。结果：热化联合组ROS高于对照组和单纯化疗组,NAC可抑制其表达（P〈0.05）,SP600125和Wortmannin对其没影响（P〉0.05）;JNK磷酸化水平在热化联合组升高,NAC使其磷酸化水平降低（P〈0.05）;Akt磷酸化水平在热化联合组表达降低,NAC使其磷酸化水平升高（P〈0.05）;热化联合组细胞凋亡率升高,Wortmannin组细胞凋亡率增加,SP600125组和NAC组细胞凋亡率减少（P〈0.05）。结论：热化疗联合诱导ROS产生,通过激活JNK信号转导通路和抑制Akt通路的激活,导致细胞凋亡。

英文摘要：

Objective To study the possible mechanisms of inhibitory effect of thermo-chemotherapy on lung neoplasm and the effect of ROS in it. Methods H446 cells were subjected to 6 thermo-chemotherapy strategies and cells without any treatment were used as the control. ROS was detected with fluorescence. Phosphorylation of JNK and Akt were determined by Western blotting. Cell apoptosis was analyzed by flow cytometry. Results The production of ROS was higher in the thermo-chemotherapy group than that in the other groups, which could be inhibited by NAC （P 0.05）; Phosphorylation of JNK was significantly increased in the thermo-chemotherapy group and decreased in SP600125 and NAC groups（P 0.05）; Phosphorylation of Akt significantly decreased in the thermo-chemotherapy group, which could be blocked by Wortmannin, but increased by NAC （P 0.05）; The rate of cell apoptosis was the highest in the thermo-chemotherapy group, which increased in Wortmannin group and decreased in SP600125 and NAC groups （P 0.05）. Conclusions Thermo-chemotherapy showed a stronger inhibitory effect than chemotherapy alone on lung tumor cell growth, probably through induction of ROS production and subsequent activation of JNK and inhibition of Akt phosphorylation, leading to cell apoptosis.