- Author:
	        		
		        		
		        		
			        		Tae Myoung KIM
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Sang Kyung SHIN
			        		
			        		;
		        		
		        		
		        		
			        		Tae Wang KIM
			        		
			        		;
		        		
		        		
		        		
			        		So Young YOUM
			        		
			        		;
		        		
		        		
		        		
			        		Dae Joong KIM
			        		
			        		;
		        		
		        		
		        		
			        		Byeongwoo AHN
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Original Article ; Research Support, Non-U.S. Gov't
 - Keywords: apoptosis; elm tree extract; HepG2 cell; Ulmus davidiana
 - MeSH: 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
 - From:Journal of Veterinary Science 2012;13(1):7-13
 - CountryRepublic of Korea
 - Language:English
 - 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.
 
            
