Elm tree bark extract inhibits HepG2 hepatic cancer cell growth via pro-apoptotic activity
Journal of Veterinary Science
; : 7-13, 2012.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-13098
Responsible library:
WPRO
ABSTRACT
Control of inflammation is widely accepted as an important strategy for cancer chemoprevention. Anti-inflammatory effects of bark extracts of elm tree (BEE) have been amply reported. Therefore, BEE may be a good candidate cancer chemopreventive agent. Considering the high incidence of hepatic cancer and limited therapeutic approaches for treating this disease, it is important to develop liver cancer-specific chemopreventive agents. To evaluate the chemopreventive potential of BEE, we investigated the growth inhibition effect of BEE on the HepG2 human hepatocellular carcinoma cell line. We performed a cell counting kit-8 assay to determine cell viability, and 4,6-diamino-2-phenylindole staining and flow cytometry to measure apoptotic cell death. Finally, the expression levels of pro- and anti-apoptotic proteins were measured. BEE inhibited the growth of HepG2 cells and induced apoptosis in a dose-dependent manner. Pro-apoptotic activity was promoted via the mitochondrial pathway of apoptosis, as demonstrated by the activation of pro-apoptotic proteins Bax, caspase-9, caspase-3, and poly (ADP-ribose) polymerase as well as the down-regulation of the anti-apoptotic protein Bcl-2. These results suggest that BEE may have potential use in hepatic cancer chemoprevention by suppressing cancer cell growth via pro-apoptotic activity.
Full text:
Available
Health context:
SDG3 - Target 3.4 Reduce premature mortality due to noncommunicable diseases
Health problem:
Digestive System Diseases
/
Liver Cancer
Database:
WPRIM (Western Pacific)
Main subject:
Plant Extracts
/
Cell Survival
/
Blotting, Western
/
Poly(ADP-ribose) Polymerases
/
Apoptosis
/
Carcinoma, Hepatocellular
/
Plant Bark
/
Ulmus
/
Bcl-2-Associated X Protein
/
Caspase 3
Limits:
Humans
Language:
English
Journal:
Journal of Veterinary Science
Year:
2012
Document type:
Article