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作 者:刘晓燕[1] 王丽[1] 郑勇[2] 何涛[1] 段承刚[1]
机构地区:[1]泸州医学院医学分子生物学实验室,泸州646000 [2]泸州医学院显微镜室
出 处:《现代预防医学》2011年第8期1497-1499,共3页Modern Preventive Medicine
基 金:四川省卫生厅资助项目(060065)
摘 要:[目的]研究去乙酰化转移酶抑制剂TSA对人肝癌HepG2细胞的作用及其FHIT表达的影响。[方法]培养的人肝癌HepG2细胞随机分为两组:对照组给予等量DMSO,实验组给予终浓度分别为125、250、500、1 000、2 000nmol/L的TSA,培养24 h后收集细胞,MTT比色法检测细胞活性,TUNEL法检测细胞凋亡率,逆转录聚合酶链反应(RT-PCR)和免疫细胞化学检测FHIT的mRNA和蛋白表达水平。[结果]与对照组相比,经TSA处理的细胞增殖速度明显减慢,TUNEL阳性细胞百分率随TSA浓度的升高呈剂量依赖性增高(P﹤0.01),细胞FHIT mRNA表达增强(P﹤0.01),FHIT蛋白表达差异具有统计学意义(P﹤0.01)。[结论]TSA可能通过抑制HDACs的活性,上调FHIT表达,诱导细胞凋亡而抑制肝癌细胞生长。[Objective]To study the role of histone deacetylase inhibitors(TSA)to the human hepatoma cell line HepG2 and the effect of fragile histidine triad(FHIT)expression.[Methods]Cultured cells were divided into control group and experimental group at random,which given with DMSO and TSA(125,250,500,1 000 and 2 000 nmol/L)respectively.24 hours later the cells were collected.The effect of TSA on the activity of cells was observed by MTT.Apoptosis index was determined by using TUNEL technique and the expression of FHIT was analyzed by using RT-PCR and immunocytochemistry.[Results]Compared with control group,the proliferation of HepG2 cell was inhibited significantly after the treatment of TSA.Apoptosis index significantly increased(P﹤0.01),and the expression of FHIT mRNA and protein were significantly increased(P﹤0.01).[Conclusion]Histone deacetylase inhibitor TSA could inhibit the proliferation of HDACs,which may be related to the change of FHIT and apoptosis.
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