目的：探讨莱菔硫烷（sulforaphane, SFN）诱导人肝癌 HepG-2 细胞凋亡过程中，p38MAPK 途径的作用。方法：流式细胞仪检测 SFN 对 HepG-2 细胞凋亡率的影响，Western Blotting 方法检测细胞内 p38 及 p-p38 蛋白表达。结果：SFN可明显诱导 HepG-2 细胞凋亡，10、20、40 μmol/L SFN 作用 48 h 后，对 HepG-2 细胞的抑制率分别达到 27.42 %、46.53 %、58.92 %；10、20、40 μmol/L 的 SFN 可上调 HepG-2 细胞内 p-p38 蛋白的表达，而对 p38 的表达无明显影响。结论：SFN 可诱导 HepG-2细胞的凋亡，而且这一过程与阻断 p38MAPK 途径有关。

Objective: To investigate the roles of p38 mitogen/activated protein kinase in the apoptosis induced by sulforaphane（SFN）in HepG-2 cells. Methods: Annexin V-FITC staining was used to observe the morphology of apoptotic cells treated with different dosages of SFN for 48 h. Western Blotting was employed to detect the expression of p38 and p-p38 proteins. Results: SFN could obviously induce the cell apoptosis of HepG-2 cells and the apoptotic rate after treated with SFN at the dosage of 10, 20, and 40 μmol/L was 27.42 %, 46.53 %, and 58.92 %, respectively. Western Blotting pointed that the expression of p-p38 proteins was evidently reduced by SFN（P < 0.05）, meanwhile, there was no remarkable change on the expression of p38 protein. Conclusion: SFN could induce the cell apoptosis of HepG-2 cells by interdicting p38MAPK pathway in HepG-2 cells.

国家自然科学基金项目（30300284）；黑龙江省自然科学基金项目（D200802）；黑龙江省骨干教师项目（1154G36）