Liu Xiaoyan,Li Jing,Wang Jianwei,Jiang Rong,Chen Dilong.Total saponins of panax ginseng suppress proliferation and improve apoptosis of leukemia KG1α cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(24):2599-2603.
Liu Xiaoyan,Li Jing,Wang Jianwei,Jiang Rong,Chen Dilong.Total saponins of panax ginseng suppress proliferation and improve apoptosis of leukemia KG1α cells[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(24):2599-2603.DOI:
Objective To investigate the effect of total saponins of panax ginseng (TSPG) on the proliferation of acute myelocytic leukemia KG1α cells. Methods The density of KG1α cells with logarithmic phase were regulated to 5×10
8/L
and incubated wit
h 0.1
0.2
0.4
0.6
and 0.8 g/L TSPG respectively. The conventional culture was carried out in the blank control group. The effects of TSPG on the proliferation of KG1a cells were examined by MTT assay. Morphological alterations of KG1a cells were observed by light microscopy and electron microscopy. The effect of TSPG on KG1a cell cycle and apoptosis were determined by flow cytometry (FCM). Expression of β-catenin and NF-κB p65 protein was detected by immunohistochemistry. Expressions of β-catenin and NF-κB p65 mRNA were detected by RT-PCR. Results TSPG inhibited KG1α cells proliferation significantly in vitro in a dose-dependent manner at range of 0.1 to 0.8 g/L. And the efficiency reached its peak at the dose of 0.4 g/L for 48 h. Compared with the blank control
apoptotic cells and morphologic changes were found under microscope after the cell were treated with 0.4 g/L TSPG for 48 h. The analysis of cell cycle showed that there was no significant change compared with that of the blank control (P0.05). The apoptotic rate of cells was significantly raised compared with that of the blank control (P0.05). The expressions of β-catenin and NF-κB p65 proteins were decreased in KG1α cells. The levels of mRNA of β-catenin and NF-κB p65 were declined compared with the blank control (P0.05). Conclusion TSPG inhibits the proliferation of KG1α cells by inducing apoptosis
probably by the mechanism of inhibiting the expressions of β-catenin and NF-κB at protein and mRNA levels.