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目的体外研究Caspase-3,8,9在莱菔硫烷(Sulforaphane,SFN)诱导人腺样囊性癌细胞系ACC-M凋亡中的作用,探讨其可能的机制,为临床应用SFN治疗腺样囊性癌提供理论依据。方法 ACC-M细胞经40μmol/L SFN处理4,8,16,24h后,采用分光光度法分别检测Caspase-3,8,9的活性变化。ACC-M细胞采用50μmol/L的Caspase抑制剂Z-VAD-FMK预处理2h后,加入40μmol/L SFN,设阴性和阳性对照,流式细胞术检测细胞凋亡率情况。结果 SFN诱导涎腺腺样囊性癌ACC-M凋亡过程中,Caspase-3,8,9的活性均在4小时时即出现增高,并持续到24小时,且在16小时时活性最高,各时间组与对照组相比均有统计学差异。50μmol/L Caspase抑制剂Z-VAD-FMK预处理细胞2小时,能显著抑制SFN诱导的ACC-M细胞凋亡。结论 SFN在诱导ACC-M细胞凋亡过程中,引起Caspase-3,8,9活性升高,Caspase在SFN诱导ACC-M细胞凋亡中起重要作用。
Objective To investigate the role of Caspase-3, 8, 9 in the apoptosis of human adenoid cystic carcinoma cell line ACC-M induced by sulforaphane (SFN) in vitro and to explore its possible mechanism. Cystic cancer provides a theoretical basis. Methods ACC-M cells were treated with 40μmol / L SFN for 4, 8, 16 and 24 hours, respectively. The changes of the activity of Caspase-3, 8 and 9 were detected by spectrophotometry. ACC-M cells were pretreated with 50μmol / L Caspase inhibitor Z-VAD-FMK for 2h. Then, 40μmol / L SFN was added into the ACC-M cells. Negative and positive controls were set. Flow cytometry was used to detect the apoptotic rate. Results During the apoptosis of ACC-M induced by SFN, the activity of Caspase-3, 8 and 9 increased at 4 hours and lasted for 24 hours, and reached the highest level at 16 hours. Each time group compared with the control group were statistically significant. Pretreatment of cells with 50μmol / L Caspase inhibitor Z-VAD-FMK for 2 hours significantly inhibited SFN-induced ACC-M cell apoptosis. Conclusion SFN induces the increase of Caspase-3, 8 and 9 in the process of ACC-M cell apoptosis, and Caspase plays an important role in the apoptosis of ACC-M cell induced by SFN.