摘要
目的:通过组蛋白去乙酰化酶(histone deacetylase,HDACS)抑制剂古抑菌素A(Trichostatin A,TSA)对人肝癌细胞HepG2(以下简称HepG2)和正常肝细胞LO2(以下简称LO2)增殖与凋亡作用的比较,探讨TSA对肝癌的作用机制。方法:应用光学显微镜、透射电镜、四氮唑蓝(MTT)法、免疫细胞化学法观察经不同浓度TSA处理后的HepG2和LO2的增殖、凋亡与凋亡相关蛋白的改变。结果:HepG2细胞经TSA处理后,电镜下超微结构发生了凋亡早期改变;小剂量TSA对HepG2细胞具有较强的抑制作用,对LO2细胞影响不明显,当TSA浓度达到1000nmol/L以上时,对LO2表现出明显的细胞毒性作用;TSA可诱导HepG2细胞凋亡,并增加凋亡相关蛋白Bax的表达。结论:TSA可明显抑制肝癌细胞HepG2的增殖,其机制可能与上调Bax的表达,诱导细胞凋亡有关。
Objective:To investigate the mechanism of trichostatin A (TSA) by comparing the effects of TSA on the proliferation and apotosis of human hepatocellular carcinoma HepG2 cells and normal hepatocellular LO2 cells. Methods:MTT,phase-contrast-microscope,electron-microscopy, immunocytochemistry were conducted to observe the alteration of cell proliferation, apotosis and apoptosis-related protein of HepG2 and L02 after treated with TSA.Results:The HepG2 ceils altered in their cells forms and the early apoptosis was observed under electron microscope. Low dosage TSA had a very strong inhibition to HepG2 cells, nearly no efficacy on LO2 cells. When the TSA concentration of 1000nmol/L or above,the apparent cytotoxicity appeared to LO2 cells. TSA could induce the apoptosis of HepG2 cells and increase the expressions of bax. Conclusion:TSA can inhibit the proliferation of HepG2 cells. This maybe related to cell apoptosis by upmodulating the expression of Bax.
出处
《现代医药卫生》
2010年第15期2248-2250,共3页
Journal of Modern Medicine & Health
基金
四川省卫生厅科研项目
编号:060065