刺五加多糖通过ERK信号转导途径诱导H446细胞G_2/M期阻滞

ASPS induces G_2/M arrest of H446 cells by activation of ERK signal pathway

目的研究刺五加多糖(ASPS)对人小细胞肺癌H446细胞G2/M期阻滞的诱导作用及对ERK信号传导途径的影响。方法流式细胞技术(FCM)检测H446细胞周期;Western blot分析检测ASPS对ERK、p-ERK蛋白的影响。结果与对照组相比,各ASPS处理组G2/M期细胞所占的比例明显增高(P<0.01),G0/G1期细胞所占的比例没有差异;加入ERK抑制剂PD98059后,G2/M期和G0/G1期细胞所占的比例与对照组没有差异;p-ERK的量显著高于对照组(P<0.01),而对ERK蛋白表达没有明显影响。结论ASPS可能通过激活ERK信号转导途径诱导H446细胞发生G2/M期阻滞。

Objective To investigate ASPS induced G2/M arrest in lung cancer cell line H446 and its effect on ERK MAP kinase signal transduction pathways. Methods Cell cycle phases were inspected by flow cytometery （FCM） ; Western blot analysis was used to inspect the proteins of ERK, p-ERK. Results Compared with control group, G2/M phase cells increased with concentration significantly, G0/G1 phase cells were not different, G2/M phase cells and G0/GE phase cells were not different when pre-incubated with PD98059 prior to exposure to ASPS of different concentrations, protein of p-ERK was significantly increased, expression of ERK was no different. Conclusion ASPS may induce G2/M arrest of H446 cells possibly by activation ERK MAP kinase pathways.