摘要
目的:研究芍药苷诱导人肝癌细胞株HepG-2细胞凋亡的作用及机制。方法:采用人肝癌细胞株HepG-2细胞药理学方法,观察芍药苷对HepG-2细胞凋亡及凋亡相关调控基因Bax、Bcl-2及抑癌基因P53表达的影响。结果:芍药苷2mg/mL对HepG-2细胞增殖均有显著抑制作用(31.45%),其细胞凋亡率(21.67%)显著高于无药对照组(3.06%)。芍药苷上调凋亡调控基因Bax、P53的表达,与无药对照组比较,差异显著,且呈剂量依赖关系,P<0.05。结论:芍药苷能在一定程度上抑制HepG-2细胞的增殖和诱导其凋亡,其作用机理之一可能是上调促凋亡基因Bax和P53的表达。
Objective : In order to seek some active which are safety and efficacious in the therapy of liver neoplasmas, through studying the action of paeoniflorin on inducing human hepatocarcinoma cell strain HepG -2 to apoptosis in vitro and primarily investigating the mechanism the mechanism of that action. Methods :The model of human hepatocarcinoma cell strain HepG - 2 and the technique of cytopharmacology were adopted. Effects of paeoniflorin on apoptosis of HpeG - 2 and correlative apoptosis regulator Bax and Bel - 2 gene were observed by contrast. Results : ( 1 ) The three efficacious concentrations as 2mg/mL, l mg/mL, and 0.5mg/mL of Paeoniflorin could obviously inhibitHepG -2 cell multiplication (P 〈 0.01 ). (2) Apotosis rate was 21.67% in 2mg/mL Paeoniflorin treat - groups correspondingly, and the differences were remarkable in comparison with which in non- drug control- gronp( P 〈0.05). Conlusion :Paeoniflorincan inhibit HepG - 2 to acertain degree. Paeoniflorin have action on inducing HepG - 2 to apoptosis. That up - regulating the expression of Bax gene as an apoptosis accelerator is probably one mechanism of htat action.
出处
《中华中医药学刊》
CAS
2007年第7期1346-1347,共2页
Chinese Archives of Traditional Chinese Medicine
基金
国家自然科学基金(30271562
30371787)
国家科技部重大基础研究资助项目(2002CCC00300)
湖北省自然科学基金(2001ABB17)
湖北省教育厅"十五"重大研究项目(2002D00003)
湖北省卫生厅科研基金资助项目(2000138)