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Transplant Proc ; 56(2): 448-452, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38368128

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.


Subject(s)
Furans , Lignans , Melanoma, Experimental , Vascular Endothelial Growth Factor A , Animals , Humans , Vascular Endothelial Growth Factor A/pharmacology , Cell Line, Tumor , Apoptosis , Melanoma, Experimental/metabolism , Proto-Oncogene Proteins c-bcl-2/metabolism , Proto-Oncogene Proteins c-bcl-2/pharmacology , Cell Proliferation
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