Arctigenin Induces Apoptosis in Melanoma Cells by Reducing the Expression of BCL-2 and VEGF

Abstract

Background: To investigate the biological effects of arctigenin on B16-F10 melanoma cells in vitro and to explore its mechanism.

Methods: B16-F10 melanoma cells in vitro were treated with the blank control solution and arctigenin solution of different concentrations, respectively. Cell proliferation and apoptosis were analyzed using the CCK-8 assay and cell loss assay, and the effect of arctigenin on melanoma cell proliferation was evaluated. Western blot was used to analyze the expression of BCL-2 protein and vascular endothelial growth factor (VEGF) in the cells of different groups and to explore the mechanism of action of arctigenin.

Results: The proliferation rate of B16-F10 melanoma cells treated with arctigenin solutions was significantly lower than that of the blank control group (P < .05), and the proliferation rate decreased with increasing concentration of arctigenin. The apoptosis rate of B16-F10 melanoma cells treated with arctigenin solutions was significantly higher than that of the blank control group (P < .05), and the apoptosis rate increased with increasing concentration of arctigenin. The expression levels of BCL-2 and VEGF in B16-F10 melanoma cells treated with arctigenin solutions were significantly lower than those in the blank control group (P < .05), and the expression levels decreased as the concentration of arctigenin increased.

Conclusions: Arctigenin can inhibit the proliferation and promote the apoptosis of melanoma cells, and the mechanism may be associated with decreasing the expression of BCL-2 and VEGF in melanoma cells.