曲古抑素A激活FAS途径促使A549/CDDP细胞凋亡  

TSA prompts A549/CDDP cell apoptosis by activating FAS-pathway

作　　者：伍俊[1] 易震南[1] 胡成平[2] 

机构地区：[1]广东医学院呼吸疾病研究所,广东湛江524023 [2]中南大学湘雅医院呼吸内科,长沙410008

出　　处：《重庆医学》2011年第23期2294-2296,I0001,共4页Chongqing medicine

摘　　要：目的探讨曲古抑素A(TSA)是否可以诱导FAS的表达,促进人肺腺癌耐顺铂细胞株A549/CDDP细胞凋亡,揭示TSA诱导A549/CDDP细胞凋亡的可能机制。方法 Hoechst 33258荧光染色观察细胞凋亡,流式细胞仪检测细胞凋亡和细胞周期变化,间接免疫荧光检测FAS表达,蛋白印迹法检测FAS、半胱氨酸天冬氨酸蛋白酶8(caspase-8)表达变化。结果 TSA诱导A549/CDDP细胞凋亡,流式细胞仪检出凋亡率由3.9%递增至21.7%。procaspase-8被激活,FAS表达呈浓度和时间依赖性上调。结论 TSA诱导A549/CDDP细胞凋亡可能与死亡受体介导的途径相关。Objective To investigate the effect of trichostatin A（TSA）on FAS-dependent pathway for studying the mechanism of TSA-induced A549/CDDP cell apoptosis.Methods Cell apoptosis was analyzed by Hoechst 33258 fluorescence dye and flow cytometry.The changes of Caspases-8 and FAS in A549/CDDP cells were detected with Western blotting and indirect immunofluorescence assay.Results After treatment with TSA,A549/CDDP cells showed typical apoptotic morphological character.Using flow cytometry,the apoptotic percentage increased from 3.9% to 21.7%.The level of FAS increased and the hydrolysis of procaspase-8 increased in a time and dose-dependent manner.Conclusion TSA-induced apoptosis may be associated with death receptors pathway.

关 键 词：曲古抑素A 细胞凋亡 FAS 半胱氨酸天冬氨酸蛋白酶8 

分 类 号：R734.2[医药卫生—肿瘤]