目的：探討萊菔硫烷（sulforaphane, SFN）誘導(dǎo)人肝癌 HepG-2 細(xì)胞凋亡過(guò)程中，p38MAPK 途徑的作用。方法：流式細(xì)胞儀檢測(cè) SFN 對(duì) HepG-2 細(xì)胞凋亡率的影響，Western Blotting 方法檢測(cè)細(xì)胞內(nèi) p38 及 p-p38 蛋白表達(dá)。結(jié)果：SFN可明顯誘導(dǎo) HepG-2 細(xì)胞凋亡，10、20、40 μmol/L SFN 作用 48 h 后，對(duì) HepG-2 細(xì)胞的抑制率分別達(dá)到 27.42 %、46.53 %、58.92 %；10、20、40 μmol/L 的 SFN 可上調(diào) HepG-2 細(xì)胞內(nèi) p-p38 蛋白的表達(dá)，而對(duì) p38 的表達(dá)無(wú)明顯影響。結(jié)論：SFN 可誘導(dǎo) HepG-2細(xì)胞的凋亡，而且這一過(guò)程與阻斷 p38MAPK 途徑有關(guān)。

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.

國(guó)家自然科學(xué)基金項(xiàng)目（30300284）；黑龍江省自然科學(xué)基金項(xiàng)目（D200802）；黑龍江省骨干教師項(xiàng)目（1154G36）