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.
Apoptosis/*drug effects ; Blotting, Western ; Carcinoma, Hepatocellular/*drug therapy/metabolism/pathology ; Caspase 3/metabolism ; Caspase 9/metabolism ; Cell Survival/drug effects ; Flow Cytometry ; Hep G2 Cells ; Humans ; Indoles/chemistry ; Liver Neoplasms/*drug therapy/metabolism/pathology ; Plant Bark/chemistry ; Plant Extracts/*pharmacology ; Poly(ADP-ribose) Polymerases/metabolism ; Ulmus/*chemistry ; bcl-2-Associated X Protein/metabolism