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目的研究N-乙酰半胱氨酸(NAC)对钚-238(238Pu)α粒子辐射致肺癌细胞模型BERP35T-1细胞内活性氧自由基(ROS)水平以及细胞增殖和迁移的影响。方法用不同浓度NAC(0～10 mmol/L)作用BERP35T-1细胞72 h后,以及BERP35T-1细胞经1 mmol/L NAC作用不同时间(0～72 h)后,二苯基溴化四氮唑蓝(MTT)法检测细胞增殖情况;DCFH-DA荧光探针标记结合荧光显微镜观察实验和细胞划痕愈合实验分别检测人支气管上皮细胞BEP2D、BERP35T-1细胞以及1 mmol/L NAC作用BERP35T-1 48 h后细胞内ROS水平和细胞的迁移能力。结果 1～10 mmol/LNAC作用BERP35T-1 72 h后,以及1 mmol/L NAC作用BERP35T-1 24～72 h后,细胞增殖受到显著抑制(P<0.01)。与BEP2D细胞比较,BERP35T-1细胞内ROS水平明显升高(P<0.01),细胞的迁移能力明显增强(P<0.01);1 mmol/LNAC作用BERP35T-1 48 h后,细胞内ROS水平显著降低(P<0.01),细胞的迁移能力显著减弱(P<0.01)。结论抗氧化剂NAC可显著抑制人支气管上皮细胞α粒子辐射致癌模型BERP35T-1的恶性增殖和迁移,作用机制可能与其降低细胞内基础ROS水平有关。
Objective To investigate the effects of NAC on the activity of reactive oxygen species (ROS) and cell proliferation and migration of BERP35T-1 cells induced by plutonium-238 (238Pu) α in lung cancer cells. Methods After treated with different concentrations of NAC (0 ~ 10 mmol / L) for 72 h, and BERP35T-1 cells treated with 1 mmol / L NAC for different times (0 ~ 72 h) The proliferation of BEP2D and BERP35T-1 cells and the effect of 1 mmol / L NAC on the proliferation of human bronchial epithelial cells, BERP35T and DCPH, were detected by MTT assay and fluorescence microscopy (DCFH-DA) -1 48 h after intracellular ROS levels and cell migration. Results The proliferation of BERP35T-1 cells was significantly inhibited after 1 ~ 10 mmol / L NaCl treatment for 72 h and BERP35T-1 1 mmol / L NAC treatment for 24 ~ 72 h (P <0.01). Compared with BEP2D cells, ROS level in BERP35T-1 cells was significantly increased (P <0.01) and cell migration was significantly enhanced (P <0.01). After treated with 1 mmol / L NaCl for 48 h, ROS levels in BERP35T- (P <0.01), and the migration ability of cells was significantly weakened (P <0.01). Conclusion Antioxidant NAC can significantly inhibit the malignant proliferation and migration of BERP35T-1, an oncogenic model induced by α-particle in human bronchial epithelial cells, and its mechanism may be related to the decrease of intracellular ROS level.