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Objective:To evaluate the inhibitory effect of dihydroartemisinin on neuroblastoma cell line SH-SY5 Y,explore the possible mechanism of dihydroartemisinin against neuroblastoma cells.Methods:The cell viability of dihydroartemisinin treated SH-SY5 Y cells was examined by MTT assay and morphology of cells was observed by using inverted microscope.Cell cycle was examined with flowcytometry assay,then cyclin D1 and caspase-3 proteins expression was detected by ELISA and western blotting assay.Results:MTT analysis results showed that cell viability significantly decreased after exposure to 0.05,0.50,5.00 and 50.00 mmol/L dihydroartemisinin in a dose-dependent manner,and the lower density of cells was observed in treated groups.The number of cells in sub-G1 phase was increased after treatment with different doses of dihydroartemisinin compared with the control group.The expression of cyclin D1 protein was decreased,while the expression of caspase-3 protein was increased in treated group.Conclusions:Dihydroartemisinin could inhibit the proliferation through stopping the cell cycle and inducing the apoptosis in neuroblastoma SH-SY5 Y cells.
Objective: To evaluate the inhibitory effect of dihydroartemisinin on neuroblastoma cell line SH-SY5 Y, explore the possible mechanism of dihydroartemisinin against neuroblastoma cells. Methods: The cell viability of dihydroartemisinin treated SH-SY5 Y cells was examined by MTT assay and morphology of cells was observed by using inverted microscope. Cell cycle was examined with flow cytometry assay, then cyclin D1 and caspase-3 protein expression was detected by ELISA and western blotting assay. Results: MTT analysis results showed that cell viability significantly decreased after exposure to 0.05, 0.50 , 5.00 and 50.00 mmol / L dihydroartemisinin in a dose-dependent manner, and the lower density of cells was observed in treated groups. The number of cells in sub-G1 phase was increased after treatment with different doses of dihydroartemisinin compared with the control group The expression of cyclin D1 protein was decreased, while the expression of caspase-3 protein was increased in treated group. Con lusions: Dihydroartemisinin could inhibit the proliferation through stopping the cell cycle and inducing the apoptosis in neuroblastoma SH-SY5 Y cells.