熊去氧胆酸选择性诱导人肝癌细胞株HepG2凋亡探讨  

UDCA selectively induces human hepatocarcinoma cell line HepG2 to apoptosis

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作  者:周正斌[1] 杨大明[2] 徐静[2] 孟宪镛[2] 

机构地区:[1]江苏省泰兴市人民医院消化内科,225400 [2]南通大学附属医院消化内科

出  处:《中国现代医药杂志》2006年第10期36-39,共4页Modern Medicine Journal of China

摘  要:目的探讨熊去氧胆酸(UDCA)对人肝癌细胞株HepG2、肝细胞株QSG-7701增殖、凋亡及对Survivin、Caspase-3表达的影响。方法UDCA孵育两种细胞后,分别采用MTT法、流式细胞仪、电镜、免疫组化法等观测相关指标。结果UDCA能抑制HepG2增殖,诱导其凋亡,并具有浓度、时间依赖性。随着Survivin表达下调,Caspase-3表达上调(r=-0.9853,P<0.01)、细胞增殖抑制(r=0.9789,P<0.05)、凋亡指数增加(r=-0.9632,P<0.05)。肝细胞株QSG-7701中无Survivin表达。UDCA对肝细胞株QSG-7701增殖、凋亡无明显影响。结论UDCA可能通过干预Survivin的表达,选择性地诱导肝癌细胞株HepG2凋亡。Objective To investigate the effects of UDCA on the growth of human hepatocarcinoma cell line HepG2 and hepatic cell line QSG-7701 and to discuss the possible mechanism. Methods MTF assay, Flow cytometry (FCM),Electron microscope were used to detect the presence of apoptosis, growth activity and apoptosis rate . The express of Survivin, Caspase- 3 in the two cell lines was examined by SP immunocytochemical staining. Results Electron microscope showed the presence of apoptosis of HepG2 treated by UDCA. There was a significant positive association between growth suppression rate and the level of UDCA concentration and the duration of treatment. Apoptosis rate of treatment group (200μg/ml,24h) was (35.62± 2.56)%,control group (3.73±0.11)% (P〈0.01) :There was no apoptosis evidence of QSG-7701 treated by UDCA in the study. Conclusion UDCA is able to inhibit cell proliferation and induce apoptosis of cell line HepG2. The mechanism may possibly relate to down-regulating the expression of Survivin, and up-regulating that of Caspase-3. There is no expression of Survivin in human hepatocyte line QSG-7701.UDCA had no obvious effect on QSG-7701.

关 键 词:熊去氧胆酸 SURVIVIN CASPASE-3 凋亡 肝癌 

分 类 号:R735.7[医药卫生—肿瘤]

 

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