CAJ | 학술논문

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。
목적：관찰이류청산분을지（PEITC）유도폐암NCI-H446세포조망적분자궤제。방법：체외배양NCI-H446세포，분별용10，30화50μmol/L PEITC작용24h，MTT법화류식세포술분별검측세포적증식여조망；Western blot검측Akt린산화、세포내조망상관단백bcl-2급Bax적함량。결과：불동PEITC처리후，가현저억제NCI-H446세포증식，병유도기조망。PEITC처리후，세포내bcl-2함량현저고우대조조，동시，bax함량유소강저。PEITC야능억제NCI-H446세포중Akt적린산화수평。결론：PEITC가능통과영향PI3K/Akt적활성이발휘촉조망작용。
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.