Abstract:

Objective   To study the influence of Gambogic acid (GA) on the proliferation and cell apoptosis of chronic myeloid leukemia cells, and to investigate the possible mechanism. Methods   After treatment with various concentrations of GA, cell viability was determined by MTS assay and trypan-blue counting method. The morphologic changes of K562 cells induced by GA were observed under fluorescence microscope with Propidium Iodide (PI) staining. Cell apoptosis was analyzed by Flow Cytometry staining with AnnexinV-FTIC/PI. The changes of apoptosis and proliferation-related proteins were tested by Western blotting. Results   GA inhibited the proliferation of K562 cells in a time- and dose- dependent manner(P<0.05). After treatment with various concentrations of GA, morphological changes were observed under fluorescence microscope，and nucleus of death cells were stained red with PI. Flow Cytometry showed that the death type of the treatment group was mainly apoptosis, and the apoptosis rate significantly increased compared with the control group(P<0.05). The caspase protein was activated, and Bcr-Abl protein and downstream signal pathway were inhibited(P<0.05). Conclusion   GA could induce apoptosis and inhibit the proliferation of K562 cells．This effect may be mediated by activated caspase protein, reduced expression of Bcr-Abl protein and its downstream signal pathway.

Key words: Gambogic acid; K562 cells; Apoptosis; Bcr-Abl