Costunolide Induces Apoptosis of K562/ADR Cells through PI3K/AKT Pathway

Abstract

To explore the effects of costunolide on the proliferation and apoptosis of human chronic myeloid leukemia drug resisitant cell line K562/ADR and its mechanism. The proliferation of the cells was assessed by CCK-8 assay, while flow cytometry was used to detect the apoptosis of the cells. The related-proteins were detected by using Western blot. The proliferation of K526/ADR cells was significantly inhibited by costunolide in a dose-dependent manner (r=0.9886) after treated by 0.01, 0.1, 0.25, 0.5, 1, 2.5, 5, 10, 25, 50 and 100 μmol/L costunolide for 72 h, and IC50 value of costunolide on K562/ADR cells was about (10.86±0.99) μmol/L (P<0.05). The apoptosis of K562/ADR cells could be induced by costunolide (10 and 15 μmol/L) significantly, the rate of apoptosis was 14.80%±3.27%, 33.2%±5.03%, respectively, which in comparison with a significantly difference as compared with the control group (4.30%±0.62%) (P<0.05). Western blot showed that costunolide could down-regulated the expression of p-AKT, p-PI3K, BCL-2, and up-regulated the expression of cleaved-caspase-3, cleaved-PARP significantly. Costunolide could inhibit the proliferation and apoptosis of K562/ADR cells through regulation of PI3K/AKT pathway.