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姜黄素对HepG-2细胞增殖与凋亡的影响
引用本文:曾繁余|刘菁|袁桂峰|骆耐香.姜黄素对HepG-2细胞增殖与凋亡的影响[J].中国普通外科杂志,2013,22(4):474-478.
作者姓名:曾繁余|刘菁|袁桂峰|骆耐香
作者单位:曾繁余 (桂林医学院附属医院普外二科,广西桂林,541001); 刘菁 (桂林医学院免疫学教研室,广西桂林,541004); 袁桂峰 (桂林医学院免疫学教研室,广西桂林,541004); 骆耐香 (桂林医学院免疫学教研室,广西桂林,541004);
基金项目:广西教育厅科研资助项目(项目编号:200911LX296)
摘    要:

目的:检测姜黄素对肝癌HepG-2细胞增殖及细胞凋亡的作用,以及对核转录因子κB(NF-κB)表达的影响。方法:不同浓度(10,25,50,100 μmol/L)姜黄素处理肝癌HepG-2细胞不同时间后(16,24,48 h),采用CCK-8法检测细胞增殖抑制率;50 μmol/L的姜黄素处理HepG-2细胞24 h后,用流式细胞仪检测细胞凋亡情况;不同浓度(10,25,50,100 μmol/L)姜黄素处理肝癌HepG-2细胞24 h后,用Western blot方法检测NF-κB p65蛋白的表达。结果:姜黄素能明显抑制HepG-2细胞的增殖,并呈时间和浓度依赖性(均P<0.05);姜黄素作用后,HepG-2细胞凋亡率较对照组明显增高(P<0.05);姜黄素能浓度依赖性抑制地HepG-2细胞 NF-κB p65蛋白的表达。结论:姜黄素能抑制HepG-2细胞增殖并促进其凋亡,其机制可能系通过阻断NF-κB信号通路有关。



关 键 词:

癌,肝细胞  姜黄素  NF-&kappa  B

收稿时间:2013/1/10 0:00:00
修稿时间:2013/3/29 0:00:00

Effects of curcumin on proliferation and apoptosis of HepG-2 cells
ZENG Fanyu,LIU Jing,YUAN Guifeng,LUO Naixiang.Effects of curcumin on proliferation and apoptosis of HepG-2 cells[J].Chinese Journal of General Surgery,2013,22(4):474-478.
Authors:ZENG Fanyu  LIU Jing  YUAN Guifeng  LUO Naixiang
Institution:(1. Second Department of General Surgery, the Affiliated Hospital, Guilin Medical University, Guilin, 541001, China|2. Department of Immunology, Guilin Medical University, Guilin 541004, China)
Abstract:

Objective: To investigate the effect of curcumin on the proliferation and apoptosis, as well as on expression of nuclear factor κB (NF-κB) in human hepatocellular carcinoma HepG-2 cells. Methods: The inhibition rate of cell proliferation was determined by CCK-8 assay after HepG-2 cells were exposed to different concentrations of curcumin (10, 25, 50 and 100 μmol/L) for different time periods (16, 24 and 48 h). Cell apoptosis was detected by flow cytometry following exposure of HepG-2 cells to μmol/L curcumin for 24 h. The NF-κB p65 expression in HepG-2 cells was measured by Western blot analysis after treatment with different concentrations of curcumin (10, 25, 50 and 100 μmol/L) for 24 h. Results: Curcumin significantly inhibited the proliferation of HepG-2 cells in a time- and concentration-dependent manner (all P<0.05). The apoptosis rate of HepG-2 cells was significantly increased after curcumin treatment versus untreated HepG-2 cells (P<0.05). The NF-κB p65 expression in HepG-2 cells was down-regulated in a concentration-dependent manner after incubation with gradient concentrations of curcumin. Conclusion: Curcumin can inhibit the growth and promote apoptosis of HepG-2 cells, and the mechanism may be associated with its blockage of NF-κB pathway.

Keywords:

Carcinoma  Hepatocellular  Curcumin  NF-&kappa  B

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