目的:探讨 ERK 信号通路抑制剂 U0126 与 A549 肺腺癌细胞凋亡的关系。 方法:选用不同浓度的 ERK 信号通路抑制剂 U0126(10滋MU0126、20滋MU0126 和 40滋MU0126)作用于 A549 细胞,采用流式细胞术和 TUNEL 原位末端标记法检测细胞的凋亡情况。 结果:U0126 阻断 ERK 信号通路后,细胞凋亡率明显增加,各实 验组明显高于对照组(P<0. 01),但20滋M U0126 组与40滋M U0126 组间无明显差异(P>0郾 05)。 结论:ERK 信号 传导通路与 A549 肺腺癌细胞的凋亡有关,但 A549 肺腺癌细胞凋亡是受多因素的调控。

To investigate the influence of extracellular signal-regulated kinase (ERK) pathway inhibitor U0126 in the process of cell apoptosis of A549 lung adenocarcinoma cell line. Methods:A549 cells were co-cultured with different concentrations of U0126 (10,20 and 40 滋M) and the cell apoptosis rate was monitored by commercial reagents of TdT-mediated dUTP Nick-End Labelling (TUNEL) and flow cytometry. Results:The apoptosis rate of the A549 cells was higher in the U0129 groups compared with that of the control group ( P < 0. 01 ) and there were no significant differences observed between the different concentration groups (P>0. 05). Conclusion:Extracellular signal-regulated kinase (ERK) pathway plays a role in the process of apoptosis in A549 lung adeno鄄 carcinoma cells,but it seems not the only determinant.

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