Schidandrin B kills tumor cells by initiating apoptosis in glioma SHG-44 cells

To observe the proliferation inhibition, cell cycle, and apoptosis of human glioma cell line SHG-44 treated with different concentration of Schidandrin B and explore the effect of Schidandrin B on glioma SHG-44 cells. Glioma SHG-44 cells were treated with Schidandrin B (0, 50, 100 or 200 μg/mL) for...

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Veröffentlicht in:Chinese journal of integrative medicine 2016-08
Hauptverfasser: Qi, Ling, Yu, Hong-Quan, Li, Yun-Qian, Jin, Hong, Zhao, Dong-Hai, Xu, Ye
Format: Artikel
Sprache:eng
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Zusammenfassung:To observe the proliferation inhibition, cell cycle, and apoptosis of human glioma cell line SHG-44 treated with different concentration of Schidandrin B and explore the effect of Schidandrin B on glioma SHG-44 cells. Glioma SHG-44 cells were treated with Schidandrin B (0, 50, 100 or 200 μg/mL) for 24, 48, 72 and 96 h, and cells were treated with vehicle as control. Viability of cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) analysis; cell cycle was examined with flow cytometry assay; apoptosis was detected with annexin V assay. Bax and caspase-3 proteins expression were checked by Western blot. MTT analysis showed that viability of glioma SHG-44 cells significantly decreased after exposure to Schidandrin B for the indicated time. Flow cytometry revealed that the number of cells in the sub G phase was increased, however, the number of cells in G /G , S and G /M phases were decreased after treatment with 50, 100 or 200 μg/mL Schidandrin B, compared with the respective control group. Annexin V analysis confirmed that apoptosis rates of the control group, 50, 100, and 200 μg/mL Schidandrin B group were 1.76%±0.47%, 13.98%±5.05%, 19.64%±5.53% and 63.28%±6.88% respectively, apoptotic rate increased significantly with dose-dependent manner, and apoptosis of cells were observed under the inverted microscope after 100 μg/mL Schidandrin B treatment. Bax and caspase-3 protein were highly expressed in Schidandrin B group compared with the control group. The apoptosis could be induced by different concentration of Schidandrin B on glioma SHG-44 cells, and the mechanism may be directly excited by Schidandrin B in glioma SHG-44 cells through activating mitochondrial pathway.
ISSN:1672-0415
1993-0402
DOI:10.1007/s11655-015-2406-9