Silibinin promotes the apoptosis of gastric cancer BGC823 cells through caspase pathway.

PURPOSE: To investigate the effects of silibinin, a natural compound, on the proliferation and apoptosis of BGC-823 gastric cancer cell line and to figure out the relevant pathways. METHODS: BGC-823 gastric cancer cells were treated with silibinin at various concentrations (0,25,50,100,150 and 200µM). Zero µM was the control group and the other concentrations were defined as the experimental groups. The effects of silibinin on the proliferation of BGC-823 gastric cancer cells were explored through methylthiazolyldiphenyltetrazolium bromide (MTT). Silibinin's toxic effects were detected through determination of the concentration of lactic dehydrogenase (LDH). Flow cytometry was performed to explore the effects of silibinin on apoptosis of these cells. Western blotting was conducted to study the relevant pathways acting on the BGC-823 cells. RESULTS: MTT assay showed that with the increase in silibinin concentration and extension of exposure time, the inhibitory effect silibinin on cell proliferation was enhanced in an obvious time-dosage pattern. The results of LDH detection showed that the toxicity of silibinin to cells was enhanced in an obvious time-dosage pattern with the increase in drug concentration and extension of exposure time. Flow cytometry revealed that with the increase in drug concentration, gradual increase in the proportion of early and late of apoptotic cells took place, and the comparison between the experimental and the control group showed that the difference had statistical significance. Western blotting indicated that silibinin could upregulate the expression of mitochondrial apoptosis-associated proteins, and the difference in comparison with the control group had statistical significance. CONCLUSION: Silibinin can inhibit the proliferation of BGC- 823 gastric cancer cells, and such an inhibitory effect is time- and concentration-dependent. Additionally, silibinin can promote the apoptosis of BGC-823 gastric cancer cells, which may be realized through mitochondrial apoptosis.