异硫氰酸苯乙酯抑制PI3K/Akt通路激活从而促进肺癌细胞凋亡  

Phenethyl isothiocyanate inhibits PI3K/Akt activation to induce human lung cancer cells apoptosis

作　　者：胡军[1] 胡名松[1] 曾慰[1] 刘翔[1] 郑达扬[1] 高文奎[1] 

机构地区：[1]南华大学附属第二医院心胸外科,湖南衡阳421001

出　　处：《中医临床研究》2014年第15期131-133,共3页Clinical Journal Of Chinese Medicine

摘　　要：目的:观察异硫氰酸苯乙酯(PEITC)诱导肺癌NCI-H446细胞凋亡的分子机制。方法:体外培养NCI-H446细胞,分别用10,30和50μmol/L PEITC作用24h,MTT法和流式细胞术分别检测细胞的增殖与凋亡;Western blot检测Akt磷酸化、细胞内凋亡相关蛋白bcl-2及Bax的含量。结果:不同PEITC处理后,可显著抑制NCI-H446细胞增殖,并诱导其凋亡。PEITC处理后,细胞内bcl-2含量显著高于对照组,同时,bax含量有所降低。PEITC也能抑制NCI-H446细胞中Akt的磷酸化水平。结论:PEITC可能通过影响PI3K/Akt的活性而发挥促凋亡作用。Objective：To investigate the molecular mechanisms of PEITC on human lung cancer cells apoptosis. Methods：Human lung cancer cell line NCI-H446 line was cultured in vitro, and treated with 10, 30,50μmol/L PEITC for 24h. Cell viability and apoptosis were analyzed by MTT assay and flow cytometry respectively. Phosphorylation of Akt, activation of caspase-3 and caspase-9 in NCI-H446 cells, and expression of bcl-2 and bax were detected by Western blot. Results ：PEITC significantly reduced NCI-H446 cells proliferation in dose-dependent manner, and apoptosis was also inducted after PEITC administrated. PEITC also markedly induced expression of bcl-2 as compared with control group. And the level of bax was decreased after treatment of PEITC. Conclusion：PEITC may affect the activity of PI3K/Akt to promote apoptosis.

关 键 词：异硫氰酸苯乙酯 肺癌细胞 凋亡 

分 类 号：R735.8[医药卫生—肿瘤]