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Title: | Effect of levofloxacononone chalcone derivatives on the apoptosis and autophagy of HCC SMMC-7721 cells |
Authors: | Wang, Dayu Song, Qun |
Keywords: | Levofloxacononone chalcone derivatives HCC SMMC-7721 cell apoptosis and autophagy. |
Issue Date: | 20-Sep-2017 |
Publisher: | Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi. |
Citation: | Wang, D., & Song, Q. (2017). Effect of levofloxacononone chalcone derivatives on the apoptosis and autophagy of HCC SMMC-7721 cells. Pakistan journal of pharmaceutical sciences, 30. |
Abstract: | The aim of present research work is study the effect of levofloxacononone chalcone derivatives on apoptosis and autophagy of HCC SMMC-7721 cells in patients with hepatocellular carcinoma (HCC). The HCC SMMC- 7721 cells in the logarithmic phase growth were inoculated, and the proliferation of SMMC - 7721 cells was detected by MTT assay. The effect of levofloxacononone chalcone derivatives on SMMC- 7721 cell cycle and apoptosis rate was detected by flow cytometry. Cells were treated by autophagy inhibitor chloroquine to validate the effect of levofloxacononone chalcone derivatives on cell proliferation and apoptosis. Levofloxacononone chalcone derivatives could significantly inhibit the proliferation of SMMC-7721 cells. Compared with the control group, the apoptosis rate of cells treated with levofloxacononone chalcone derivatives was increased significantly in 24h, showing significant difference between groups. Chloroquine could increase the inhibitory effect of low-dose levofloxacononone chalcone derivatives on SMMC7721 cell proliferation, and decrease the inhibitory effect of high-dose levofloxacononone chalcone derivatives on SMMC-7721 cell proliferation. Levofloxacononone chalcone derivatives can obviously induce the apoptosis and autophagy of SMMC -7721 cells, at a low dose, its autophagy can protect cells; and at a high dose, the autophagy can decrease the cell proliferation rate, to promote cell apoptosis. |
URI: | http://142.54.178.187:9060/xmlui/handle/123456789/14041 |
ISSN: | 1011-601X |
Appears in Collections: | No.5(Special), September, 2017 |
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