异硫氰酸苯乙酯诱导胆管癌细胞凋亡和细胞周期阻滞的实验研究

目的:探讨异硫氰酸苯乙酯(PEITC)对人胆管癌QBC-939细胞凋亡和细胞周期的影响。方法:PEITC处理QBC-939细胞后,采用MTT法检测细胞活力;运用流式细胞技术检测细胞凋亡率;Hoechst33342染色后荧光显微镜下观察凋亡细胞的形态;使用流式细胞技术检测细胞周期。设置对照组:加入和药物等体积的DMSO。结果:20、30、40、50μmol/L的PEITC作用于QBC-939细胞24 h后,细胞活力分别为(88.07±2.40)%、(68.02±4.04)%、(52.57±1.91)%、(36.37±3.42)%,较对照组明显降低(P<0.05);30μmol/L的PEITC处理QBC-939细胞12、18、24、48 h后,细胞活力分别为(90.74±2.96)%、(78.22%±4.85)%、(69.67±4.58)%、(40.48±2.59)%,较对照组明显降低(P<0.05)。QBC-939细胞经30μmol/L和50μmol/L的PEITC作用处理24 h后,细胞凋亡率分别为(30.51±2.77)%、(58.62±3.75)%,较对照组显著升高(P<0.05);G2/M期的细胞比例从(5.06±1.86)%上升到(16.96±2.71)%、(26.68±1.85)%,差异有统计学意义(P<0.05)。结论:PEITC可通过诱导细胞凋亡和细胞周期阻滞而发挥抗胆管癌作用,并具有时间-剂量依赖性。

Experimental study of phenethyl isothiocyanate inducing apoptosis and cell cycle arrest of cholangiocarcinoma cell

Objective： To investigate the effect of phenethyl isothiocyanate （PEITC） on the apoptosis and cell cycle in human cholangiocarcinoma cell QBC-939. Methods： After the human cholangiocarcinoma cell QBC-939 was treated with PEITC, the cell viability was detected by MTT, the apoptosis rate and cell cycle were detected by flow cytometry, the morphological change of apoptotic cells was observed under fluorescence microscopy after treated with Hoechst33342. Re, suits： Under the treatment with 20, 30, 40, 50 μ mol/L PEITC for 24 hours, the cell viability of QBC-939 cells were respectively （88.07 ± 2.40）%, （68.02 ± 4.04）%, （52.57 ± 1.91）%, （36.37 ± 3.42）% and significantly lower than the control group （P〈0.05）. After treatment with 30 μ mol/L PEITC for 12,18,24,48 hours, the cell viability were respectively （90.74 ± 2.96） %, （78.22 ± 4.85） %, （69.67 ± 4.58）%,（40.48 ± 2.59）% andsignificantly lower than the control group （P〈0.05）.The apop-tosis rates after treatment with 30 μmol/L and 50 IJ mol/L PEITC for 24 hours were respectively （30.51 ± 2.77）%, （58.62 ± 3.75）%and obviously higher than the control group （P〈O.05）, meanwhile the ratio of cells in G2/M phase increased from（5.06 ± 1.86）% to （16.96 ± 2.71 ）%,（26.68 ± 1.85）% （P〈O.05）. Conclusion： PEITC may inhibit the growth of bile duct carcinoma cell through inducing apoptosis and cell cycle arrest, in a manner of dose-and time-dependent.