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收集2×106个A 549肺腺癌细胞,以含10%胎牛血清培养后,随机分为观察组及对照组各1×106个细胞,观察组分别加入0.1、0.2、0.5μm o l/L浓度的曲古抑菌素A(TSA),对照组不予处理。观察两组A 549细胞凋亡、细胞周期及caspase-8、caspase-9表达情况。结果观察组A 549细胞凋亡率明显高于对照组,呈现时间、浓度依赖性效应关系,药物作用后72 h,0.5μm o l/L TSA处理的A 549细胞凋亡率最高,达50%;而对照组A 549细胞凋亡率在各时间点均无明显变化。观察组细胞主要积聚在G2/M期,呈浓度依赖性,0.1、0.2、0.5μm o l/L的TSA处理后,细胞积聚在G2/M期的比例分别为23.4、35.8、39.7,与对照组比较P均<0.05。W estern b lot检测证实,TSA诱导了A 549肺腺癌细胞caspase-8、caspase-9裂解活化,随着TSA作用时间延长,其蛋白着色深度逐步升高。证实TSA可诱导A 549细胞株凋亡,其机制可能为触发一种存在于正常细胞的G2检测点功能,引发cas-pase蛋白酶的级联反应。
A total of 2 × 106 A549 lung adenocarcinoma cells were collected and cultured in 10% fetal bovine serum. The cells were randomly divided into observation group and control group with 1 × 106 cells. The observation group was given 0.1, 0.2, 0.5μmol / L Trichostatin A (TSA) concentrations were not observed in the control group. Apoptosis, cell cycle, caspase-8 and caspase-9 expression in A 549 cells in both groups were observed. Results The apoptotic rate of A 549 cells in the observation group was significantly higher than that in the control group, showing a time-dependent and concentration-dependent manner. The apoptotic rate of A 549 cells treated with 0.5 μmol / L TSA for 72 h was the highest (50%). However, the apoptosis rate of A 549 cells in control group showed no significant changes at all time points. The cells in observation group mainly accumulated in G2 / M phase in a concentration-dependent manner. After TSA treatment at 0.1, 0.2 and 0.5μm ol / L, the cells accumulated in G2 / M phase were 23.4, 35.8 and 39.7, respectively. Compared with control group All P <0.05. Western blot analysis confirmed that TSA induced the cleavage of caspase-8 and caspase-9 in A 549 lung adenocarcinoma cells. With the prolongation of TSA, the protein staining depth gradually increased. Confirmed that TSA can induce apoptosis in A 549 cell line, the mechanism may trigger a function of G2 detection point existing in normal cells, trigger Cas-pase protease cascade.