Study on the Effects and Mechanism of Celastrol on Proliferation and Apoptosis of Human Hepatoma HepG2 Cells in vitro
10.6039/j.issn.1001-0408.2017.10.12
- VernacularTitle:雷公藤红素对体外人肝癌HepG2细胞增殖、凋亡的影响及机制研究
- Author:
Yan ZHANG
;
Chenchen ZHU
- Keywords:
Celastrol;
Human hepatoma HepG2 cells;
Proliferation;
Apoptosis;
Mitochondrial permeability;
in vitro
- From:
China Pharmacy
2017;28(10):1342-1345
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the effects of celastrol on the proliferation and apoptosis of human hepatoma HepG2 cells, and investigate its mechanism. METHODS:CCK-8 method was used to determine the cell activity 24,48,72 h after treated by 2, 5,10 μmol/L celastrol,and the proliferation inhibition rate and half inhibitory concentration(IC50)were calculated;flow cytome-try was conducted to detect the cell apoptosis rate and cycle change 24 h after treated by 2,5,10μmol/L celastrol,and the DMSO was used as negative control;rhodamine 123 staining method was used to determine the mitochondrial membrane potential 48 h af-ter treated by 2,5,10 μmol/L celastrol,and the DMSO was used as negative control;Western blot was adopted to detect the pro-apoptotic related genes Bax and B lymphoma 2(Bcl-2)protein expressions 0,12,24,36 h after treated by 5 μmol/L celastrol. RESULTS:2,5,10 μmol/L celastrol can inhibit cell proliferation,IC50 was 5.834 μmol/L. 2,5,10 μmol/L celastrol can induce apoptosis;5,10 μmol/L celastrol can block cell in G0/G1,S phases,compared with negative control group,with significant differ-ences(P<0.05 or P<0.01),and the above effects all showing certain concentration-dependent manner. 5 μmol/L celastrol can in-crease Bax protein expression and decrease Bcl-2 protein expression after cultured for 12,24,36 h,showing certain time-depen-dent manner;compared with 0 h,there was significant difference(P<0.05 or P<0.01). CONCLUSIONS:Celastrol can obvious-ly inhibit the proliferation of human hepatoma HepG2 cells and induce their apoptosis,and the mechanism may be related with strengthening mitochondrial permeability and promoting the release of apoptosis-inducing factor.
