土贝母皂苷-Ⅱ对人肝癌细胞HepG2增殖及细胞周期的影响  被引量:9

Effects of tubeimoside-Ⅱon proliferation and cell cycle of human hepatocellular carcinoma cell line HepG2

在线阅读下载全文

作  者:晁旭[1] 赵英永[2] 魏敏慧[1] 党琳[1] 马晓军[1] 王文娟[1] 

机构地区:[1]陕西中医学院基础医学院,712046 [2]西北大学陕西省生物医药重点实验室

出  处:《江苏医药》2012年第15期1740-1742,F0002,I0001,共5页Jiangsu Medical Journal

基  金:陕西省教育厅科研计划项目(11JK0682)

摘  要:目的探讨土贝母皂苷-Ⅱ对人肝癌细胞HepG2增殖、细胞周期的影响及其抗肿瘤效应。方法用不同浓度土贝母皂苷-Ⅱ0、2、4、6、8、10、12μg/ml处理HepG2细胞后,MTT法检测细胞生长的抑制率,荧光染色和流式细胞术分别观察凋亡细胞形态和细胞周期的变化。同时,以H22肝癌小鼠模型初步探讨土贝母皂苷-Ⅱ的抗肿瘤作用。结果土贝母皂苷-Ⅱ能剂量依赖性地抑制HepG2细胞生长,24-h半数抑制剂量(IC50)为4.05μg/ml。HepG2细胞经土贝母皂苷-Ⅱ处理后,呈现典型的凋亡细胞形态,G2/M期细胞数量增加,而G0/G1期细胞数明显减少。体内抗肿瘤实验结果证明,土贝母皂苷-Ⅱ对肿瘤的生长有显著的抑制作用。结论土贝母皂苷-Ⅱ可能是通过使肿瘤细胞滞留于G2/M期,从而抑制肿瘤细胞的增殖。Objective To investigate the effects of tubeimoside- II on proliferation and cell cycle of human hepatocellular carcinoma cell line HepG2 and evaluate its anti-tumor effect in vivo. Methods After HepG2 cells were treated with different concentrations of tubeimoside-II 0, 2, 4, 6, 8, 10, 12 ug/ml, the irihibitory rate of cell growth was measured by MTT assay, and the shape of apoptotic cells and cell cycle were detected by fluorescence staining and flow cytometry, respectively. Moreover, the anti-tumor effect of tubeimoside- II in vivo was primarily evaluated by establishing hepatoceUular carcinoma model of H22 rats. Results Tubeimoside-II inhibited cell growth in a does-dependent manner and the IC50 value was 4. 05 ug/ml. After HepG2 cells were treated with tubeimoside- II, cell appearance presented typical apoptotic phenomenon with increasing cell number in G2/M phase and decreasing cell number in G0/G1 phase. Anti-tumor experiment in vivo showed that tuheimoside-II could obviously suppress tumor growth. Conclusion Tubeimoside-II can inhibit cell proliferation probably via promoting tumor cells to stagnate in G2/M phase.

关 键 词:土贝母皂苷-Ⅱ 细胞增殖 细胞周期 

分 类 号:R966[医药卫生—药理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象