Celastrol inhibits growth and induces apoptosis of human gallbladder cancer NOZ cells
10.3760/cma.j.issn.1007-8118.2016.05.015
- VernacularTitle:雷公藤红素抑制人胆囊癌NOZ细胞增殖及诱导凋亡的研究
- Author:
Xiaobin CHI
;
Lizhi LYU
;
Xiaojin ZHANG
;
Yongbiao CHEN
;
Yi JIANG
- Publication Type:Journal Article
- Keywords:
Celastrol;
Gallbladder cancer;
Cell proliferation;
Cell apoptosis
- From:
Chinese Journal of Hepatobiliary Surgery
2016;22(5):340-343
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of celastrol on the cell growth and apoptosis of human gallbladder cancer NOZ cells,and explore its potential molecular mechanism.Methods NOZ cell were cultured in vitro.And CCK-8 assay,Annexin V-FITC/PI staining method,cell cycle analysis were conducted to investigate the effects of celastrol on the growth and apoptosis of NOZ cells after being treated with drugs.The mitochondrial membrane potential and Bax and Bcl-2 protein expression level were determined by Rhodamine 123 and Western blot,respectively.Results Celastrol could inhibit NOZ cell growth,and the IC50 value was 5.3 μmol/L.Annexin-V/PI staining showed that cell apoptosis of NOZ cells were induced as the celastrol concentration increased,and the apoptosis ratio of control group was 4.4％,while the apoptosis rates of the test groups (2,5,10 p mol/L) were 7.4％,27.1％ and 43.4％,respectively.In addition,cell cycle analysis revealed that celastrol could induce G1-phase arrest.The G1-phase rate of control group was 25.6％,while the G1-phase rates of the test groups (2,5,10 μmol/L) were 36.5％,45.7％ and 92.5％,respectively.The mitochondrial membrane potential was measured after treatment with celastrol and the results indicated that the mitochondrial membrane potential was significantly decreased.Western Blot showed that the protein expression of Bax increased and Bcl-2 decreased in a time-dependent manner after treatment with celastrol.Conclusions Celastrol may inhibit cell proliferation of human gallbladder cancer NOZ cells and induce cell apoptosis partly by inducing the loss of mitochondrial membrane potential.
