Objective:Tostudy the mechanism of shikonin inducing K562 cells apoptosis. Method: MTT colorimetric assay was used to examine the proliferation inhibition of shikonin on K562 cells. Hoechst 33258 and acridine orange(AO)/ethidium bromide(EB) fluorescent staining were used to observe the morphological changes of apoptotic cell. The mRNA expression levels of B-cell lymphoma gene 2 associated X protein(Bax)

BH3 interacting domain death agonist(Bid)

B-cell lymphoma gene xL(Bcl-xL)

p53 up-regulated modulator of apoptosis(PUMA)

B-cell lymphoma gene 2 homologous antagonist(Bak)

B-cell lymphoma-w(Bcl-w) and B-cell lymphoma gene 2 associated death promoter(Bad) were detected using RT-PCR analysis. The changes of reactive oxygen species(ROS) and reduced GSH were detected using molecular probe DCFHDA and CMFDA:CMFDA

separately. Result: Shikonin(0.2-1.6 mg·L-1)inhibited K562 cell proliferation in concentration-dependent manner

and induced cell apoptosis. Typical apoptotic changes were observed in K562 cells under the shikonin(0.2-0.5 mg·L-1) treatment groups. The expression of proapoptotic protein (Bid

Bad

Bak

PUMA

Bax) was increased and antiapoptotic protein (Bcl-w

Bcl-xL) decreased. ROS formation increased

but reduced glutathione level was decreased. Conclusion: Shikonin can inhibite K562 cell proliferation and induce apoptosis through inducing oxidative stress.