Icaritin promotes the apoptosis of leukemia K562 cells
10.3760/cma.j.issn.1009-9921.2016.06.005
- VernacularTitle:淫羊藿苷促进白血病K562细胞凋亡的研究
- Author:
Liping PAN
;
Wei YUAN
- Publication Type:Journal Article
- Keywords:
Leukemia;
Icaritin;
K562 cells;
Proliferation;
Apoptosis;
PI3k-Akt signal pathway
- From:
Journal of Leukemia & Lymphoma
2016;25(6):340-343
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of the icaritin on the human cronic myeloid leukemia K562 cells. Methods The K562 cells at logarithmic growth phase were divided into the control group and the icaritin group. The cells in the control group were normally treated and the cells in the icaritin group were incubated with 8 μmol/L icaritin. Methyl thiazolyl tetrazolium (MTT) method and flow cytometry were used to examine the proliferation and apoptotic changes in the two groups after incubation for 72 h, respectively. Gene expression of p85 and Akt were detected by RT-PCR. The protein changes of p85, Akt, p-p85, p-Akt cleavage-caspase-3 and caspase-3 were detected by Western blot. Results Compared with the control group, the proliferation rate of K562 cells in the icaritin group was significantly decreased (P<0.05), however the apoptotic rate of K562 cells and the expressions of p-p85, p-Akt, cleavage-caspase-3 in the icaritin group were significantly increased (all P< 0.05), but the expressions of p85 mRNA, Akt mRNA and caspase-3 protein had no difference (all P> 0.05). Conclusion Icaritin could induce the proliferation and promote the apoptosis of K562 cell, and its mechanism may be achieved through activating the PI3K-Akt signal transduction pathway.
