Effects and mechanism of ginsenoside Rh2 on the proliferation and apoptosis of human glioma cells
- VernacularTitle:人参皂苷Rh2对胶质瘤细胞增殖、凋亡的影响及机制
- Author:
Ying LIU
1
,
2
;
Hui TAN
1
,
2
,
3
;
Jing XIA
1
,
2
;
Wei XIONG
1
,
2
,
3
;
Xuesong DENG
1
Author Information
1. Dept. of Basic Medical Science，Chongqing Three Gorges Medical College，Chongqing 404120，China
2. Chongqing Engineering Research Center of Antitumor Natural Drugs，Chongqing 404120，China
3. Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area，Chongqing 404120，China
- Publication Type:Journal Article
- Keywords:
ginsenoside Rh2;
glioma;
histone deacetylase 1;
U87 cells;
U251 cells;
proliferation;
apoptosis
- From:
China Pharmacy
2023;34(20):2471-2475
- CountryChina
- Language:Chinese
-
Abstract:
ABSTRACT OBJECTIVE To investigate the effects and mechanism of ginsenoside Rh2 on the proliferation and apoptosis in human glioma U87 and U251 cells. METHODS Using human glioma U87 and U251 cells as subjects， the proliferation and apoptosis， as well as the expression of histone deacetylase 1（HDAC1） protein and apoptosis-related proteins [B cell lymphoma-2（Bcl-2）， Bcl-2-associated X protein （Bax） and cleaved caspase-3] were detected after being treated with different concentrations of ginsenoside Rh2. RESULTS The concentrations of 10，20，30，40，50，60，70，80 μmol/L ginsenoside Rh2 could generally significantly increase the proliferation inhibition rate of U87 and U251 cells （P＜0.05 or P＜0.01）， and the half inhibitory concentrations of this component after 48 hours of action were 51.34 and 55.84 μmol/L， respectively；30，50 μmol/L ginsenoside Rh2 could increase the total apoptotic rate of both types of cells， reduced the protein expressions of HDAC1 and Bcl-2， and increased the protein expressions of Bax and cleaved caspase-3 significantly （P＜0.05 or P＜0.01）. CONCLUSIONS Ginsenoside Rh2 has a significant inhibitory effect on the proliferation of glioma cells and promotes the apoptosis of cells， which may be through reducing the expression of HDAC1 protein and activating the Bcl-2 family protein-mediated apoptosis pathway.
