Inhibitory effect of deoxyschizandrin on growth of brain glioma cells and its mechanism
10.13481/j.1671-587x.20160415
- VernacularTitle:五味子甲素对脑胶质瘤 C6细胞生长的抑制作用及其机制
- Author:
Xue CHEN
;
Yuying ZHANG
;
Yu SHAO
;
Luni ZHANG
;
Mingjie NING
;
Ying TANG
;
Ling QI
;
Yunqian LI
- Publication Type:Journal Article
- Keywords:
deoxyschizandrin;
glioma cells;
CyclinD1;
Bax/Bcl-2
- From:
Journal of Jilin University(Medicine Edition)
2016;42(4):711-715
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the inhibitory effect of deoxyschizandrin on the growth of brain glioma C6 cells, and to explore its mechanism.Methods:The rat glioma C6 cells were cultured and divided into control group,50, 100,and 200 mg·L-1 deoxyschizandrin groups.The proliferation rates of C6 cells were examined by MTT assay;the changes of cell cycles were examined by flow cytometry;the expression levels of CyclinD1,Bax,Bcl-2 and Caspase-3 proteins in supernant were detected by ELISA assay. Results:Compared with control group, the proliferation rates at 24 and 48 h in 50,100,and 200 mg·L-1 deoxyschizandrin groups were significantly decreased (P <0.01),and the proliferation rates at 72 h in 100 and 200 mg·L-1 deoxyschizandrin groups were significantly decreased (P < 0.05 or P < 0.01 ). Compared with control group, the percentage of cells at SubG1 phase in 200 mg·L-1 deoxyschizandrin group was increased (P < 0.05 ), and the percentage of cells at S phase was decreased (P <0.05).Compared with control group,the expression levels of CyclinD1 in 100 and 200 mg· L-1 deoxyschizandrin groups were decreased (P < 0.01 );the expression levels of Bax protein in deoxyschizandrin groups were increased (P < 0.05 or P < 0.01 ), and the expression level of Bcl-2 protein in 200 mg · L-1 deoxyschizandrin group was decreased (P < 0.01 ), and the Bax/Bcl-2 value in deoxyschizandrin groups were increased (P < 0.01 ); the expression level of Caspase-3 protein in 200 mg · L-1 deoxyschizandrin group was increased (P < 0.01 ).Conclusion:Deoxyschizandrin could inhibit the growth of glioma cells through down-regulating the expression levels of CyclinD1 protein and up-regulating the expression levels apoptotic factors Bax and Bcl-2.
