目的从NF-ΚB信号通路着手探讨半边旗活性物质5F诱导非小细胞肺癌NCI-H460细胞凋亡发生的机制。方法MTT法检测5F对NCI-H460细胞的生长抑制作用;用半定量RT-PCR方法检测NCI-H460细胞IΚKβ、IΚB、p65及p50mRNA表达水平的变化。结果5F抑制NCI-H460细胞的生长,其效果与5F的质量浓度和作用时间相关,24、48、72h的IC50分别为:21.40、4.52、1.02μg/mL;100μg/mL5F作用NCI-H460细胞6h后能引起IΚKβ和IΚBmRNA表达水平显著降低(P<0.05);p65和p50mRNA水平在作用3h就发生明显减少(P<0.05)。结论5F诱导NCI-H460细胞凋亡的机制可能是通过抑制核因子-ΚB(NF-ΚB)信号通路来实现的。

Objective To investigate the inhibitory mechanism of SF isolated from Pteris semipinnata on the proliferation and apoptosis induction of NCI H460 cells.The roles of NF-KB pathway in the apoptosis were explored in this study. Methods NCI H460 Cell growth inhibition mediated by 5F was detected by MTT assay.RT-PCR was Applied to examing the mRNA levels of IΚKβ，IΚB，p65，and p50. Results 5F Showed the growth inhibitory activity against NCI H460 cells with ICSO values of 21.40, 4.52, and 1.02 μg/mL for 24,48,and 72h, respectively.The mRNA expression levels of IΚKβand IΚB were significandy decreased after SF treated cells for 6h(P<0.05);The mRNA expression levels of p65 and p50 were significantly decreased after SF treated cells for 3h(P<0.05).Conclusion The mechanism for SF induction of NCI H460 cells apoptosis could be mediated by the inhibition of NF-KB pathway.

国家自然科学基金资助项目(39870900);粤港合作课题(GHP/022/06);湛江市科技计划项目资助(2008C01006)