In:
Phytotherapy Research, Wiley, Vol. 25, No. 10 ( 2011-10), p. 1519-1526
Kurzfassung:
The study aimed to evaluate the effects of β‐escin on human cholangiocarcinoma cell lines (QBC939, Sk‐ChA‐1 and MZ‐ChA‐1) and to explore its mechanisms. Cell growth, cell cycle and apoptosis were investigated, respectively, by MTT assay, single PI and FITC/PI double‐staining flow cytometry, and fluorescence microscopy. The protein expression was determined by western blotting. The study revealed that β‐escin inhibited cholangiocarcinoma cell growth in a dose‐ and time‐dependent manner, and the cell cycle of QBC939 and Sk‐ChA‐1 cells was arrested in the G2/M phase, and MZ‐ChA‐1 cells in G1 phase. Apoptosis of the three cholangiocarcinoma cell lines induced by β‐escin was associated with the collapse of the mitochondrial membrane potential and the activation of caspase‐3. The apoptotic effect of β‐escin was suppressed by pancaspase inhibitor z‐VAD‐fmk. Molecular dissection revealed that the antiapoptotic protein bcl‐2 was down‐regulated after cholangiocarcinoma cell lines were treated with β‐escin, while the protein levels of bax and p53 were unchanged. Apoptosis was accompanied by an increase in reactive oxygen species (ROS). These results suggest that β‐escin induces apoptosis of cholangiocarcinoma cells through an intrinsic mitochondrial caspase‐dependent pathway, and the increase in the bax/bcl‐2 ratio and ROS may play important roles in β‐escin‐induced apoptosis of cholangiocarcinoma cells. Copyright © 2011 John Wiley & Sons, Ltd.
Materialart:
Online-Ressource
ISSN:
0951-418X
,
1099-1573
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2011
ZDB Id:
1493490-5
SSG:
15,3
