扶正抗癌方诱导H1650细胞凋亡的分子机制

目的:观察扶正抗癌方对H1650细胞凋亡的影响,并探讨其诱导H1650细胞凋亡的分子机制。方法:以人肺腺癌细胞株H1650细胞为研究对象,用0.5,1.0,1.5,2.0,2.5,3.0 g·L~(-1)扶正抗癌方处理H1650细胞24,48,72 h,另设空白组,四氮唑蓝盐化合物(MTS)法检测细胞增殖;用0.5,1.0,1.5 g·L~(-1)扶正抗癌方处理H1650细胞24 h,另设空白组,Annexin VFITC/碘化丙啶(PI)流式细胞术检测细胞凋亡;用0.5,1.0,2.0 g·L~(-1)扶正抗癌方处理H1650细胞24 h,另设空白组,半胱氨酸蛋白酶-3/7(Caspase-3/7)活力检测试剂盒检测Caspase-3/7活力;蛋白免疫印迹法检测扶正抗癌方对pro Casapse-3,聚腺苷二磷酸-核糖聚合酶(PARP),Bcl-2相关X蛋白(Bax)表达。结果:与空白组比较,扶正抗癌方能明显抑制H1650细胞的增殖(P0.05),且呈浓度和时间依赖性。与空白组比较,扶正抗癌方明显诱导H1650细胞的早期凋亡,增强Caspase-3/7的活力(P0.05),且呈浓度依赖性。与空白组比较,扶正抗癌方明显下调pro Casapse-3和PARP的表达(P0.05),呈浓度依赖性,明显上调Bax的表达(P0.05),且呈时间依赖性。结论:扶正抗癌方可通过激活Caspase-3和Bax诱导H1650细胞的凋亡。

Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells

Objective: To observe the effects of Fuzheng Kang''ai (FZKA) decoction on apoptosis of H1650 cells and discuss its molecular mechanism in apoptosis of H1650 cells. Method: Human lung adenocarcinoma cells (H1650 cells) were used as the research objects and treated for 24, 48, 72 h with 0.5, 1.0, 1.5, 2.0, 2.5, 3.0 g · L^-1 FZKA decoction, and a blank group was set up, then cell proliferation was detected by 3- (4, 5-diethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2- (4-sulfophenyl)-2H-etrazolium, inner salt (MTS) assay. H1650 cells were treated for 24 h with 0.5, 1.0, 1.5 g · L^-1 FZKA decoction and a blank group was set up, then cell apoptosis was detected by Annexin V-FITC/PI flow cytometry analysis. H1650 cells were treated for 24 h with 0.5, 1.0, 2.0 g · L^-1 FZKA decoction and a blank group was set up, then vitality of Caspase-3/7 was detected by Caspase-3/7 vitality test kit. Simultaneously, effects of FZKA decoction on the expression levels of proCasapse-3, PARP and Bax were detected by Western blot assay. Result: As compared with the blank group, proliferation of H1650 cells was significantly inhibited by FZKA decoction in concentration-dependent and time-dependent manners (P<0.05). As compared with the blank group, early apoptosis of H1650 cells was significantly induced and vitality of Caspase-3/7 was increased by FZKA decoction in a concentration-dependent manner (P<0.05). As compared with the blank group, the expression levels of proCasapse-3 and PARP were significantly reduced by FZKA decoction in a concentration-dependent manner (P<0.05), and the expression of Bax was increased by FZKA decoction in a time-dependent manner (P<0.05). Conclusion: Apoptosis is induced by FZKA decoction in way of activating Caspase-3 and Bax in H1650 cells.