目的: 研究莱菔硫烷对人肝癌HepG2细胞Fas、FasL、Bid蛋白表达的影响, 探讨其诱导HepG2细胞凋亡过程中Fas/FasL途径的作用。方法: Caspase-8试剂盒检测莱菔硫烷对HepG2细胞Caspase-8活性的影响; 流式细胞仪检测莱菔硫烷对HepG2细胞中Fas、FasL、Bid蛋白表达的影响。结果: 莱菔硫烷10、20、40μmol/L作用于HepG2细胞48h, 可显著升高HepG2细胞Caspase-8活性(P<0.01); 可使HepG2细胞Fas、FasL蛋白的表达显著升高(P<0.01); 莱菔硫烷20、40μmol/L时, 可显著提高Bid蛋白的表达(P<0.01), 上述作用均呈剂量相关性。结论: 激活Fas/FasL途径可能是莱菔硫烷诱导人肝癌HepG2细胞凋亡的重要机制之一。

Objective: To study the effect of sulforaphane on Fas, FasL, and Bid protein expression in HepG2 cells, and to explore the effect of Fas/FasL pathway on sulforaphane-induced apoptosis in HepG2 cells. Methods: The effect of sulforaphane on Caspase-8 activity in HepG2 cells was detected by Caspase-8 Activity Assay Kit. Flow cytometer was used to analysis of Fas, FasL, and Bid protein expression in HepG2 cells. Results: After treated by sulforaphane for 48 h, the Caspase-8 activity was effectively increased(P<0.01). At the doses of 10, 20 and 40 μmol/L, the effect of sulforaphane could significantly increase the Fas and FasL proteinexpression in HepG2 cells in a dose dependent manner, while at the doses of 20 and 40 μmol/L, sulforaphane could increase the Bidprotein expression. Conclusion: Activating the Fas/FasL pathway may be one of the role mechanism of sulforaphane inducing the apoptosis of HepG2 cells.

国家自然科学基金资助项目(30300284);黑龙江省自然科学基金重大项目(ZJY03-04D200802)