Study on pro-apoptotic effect of apigenin on human gastric cancer cells and its underlying mechanisms

Objective To determine the effect of apigenin (API) on induction of apoptotic death in human gastric cancer cells and its underlying mechanisms. Methods Human gastric cancer BGC823 cells line was cultured and treated with different concentrations of API for 48 h. Cell apoptosis and mitochondrial membrane potential was determined by flow cytometery (FCM) labeled with propidium iodide (PI) and Rhodamine123, respectively. Caspase-9 activity was determined by caspase-9 colorimetric assay kit. Western blot was used to analyze the expressions of apoptosis mitochondrial signal transduction pathway related proteins including bax, bcl-2, caspase-9 and caspase-3. Results Treatment with API (20, 40 and 80μg/mL) for 48 h could concentration-dependently induce the apoptotic death of BGC823 cells. Moreover, API could also decrease the cellular Δψm, increase the activity of caspase-9 and enhance the releasing of cytochrome c. The protein expressions of bax, caspase-9 and caspase-3 were upregulated by treatment with API, associated with a downregulation of the protein expression of bcl-2. Conclusion API can induce the apoptosis of human gastric cancer cells via activating mitochondrial signal transdution pathway.