[Mechanism of platycodin D-induced apoptosis in A549 human lung cancer cells].

ABSTRACT

OBJECTIVE: To investigate the molecular mechanism of platycodin D showing the inhibitory effect on proliferation and induced apoptosis of humane long cancer cells A549. METHOD: Humane long cancer cells A549 were cultured in vitro, with the final PD concentration of 5-20 micromol x L(-1). PD's inhibitory effect on cell proliferation was examined by MTT assay. Morphological changes in cells were observed with microscope. The cell apoptosis rate was detected by Annexin V-FITC/PI double staining. The change of mitochondrial membrane potential was detected by JC-1. The protein expressing of leaved Caspase-3, cleaved Caspase-9, cleaved PARP, Bcl-2, Bcl-xl, Bak and Bax were detected by Western blot analysis. RESULT: PD could inhibit the proliferation of A549 cells and show stronger effect with the increase of concentration and over time. Compared with the control group, PDs of different concentration showed significant increase in the cell apoptosis rate, decrease in mitochondrial membrane potential after 24 h. Protein electrophoresis inspection showed cut segments in both protein Caspase-3 and Caspase-9 and notable fractures with time. Further study found that PD decreased Bcl-2, Bcl-xl proteins and increased Bax, Bak proteins after processing A549 cells. CONCLUSION: PD shows notable effect on cytotoxicity and can induce A549 cell apoptosis. It causes decrease in mitochondrial membrane potential by regulating Bax, Bak, Bcl-2 and Bcl-xl expressions, and thus activating caspase and finally causing long cancer cell apoptosis.