- Author:
	        		
		        		
		        		
			        		Seon-Hee KIM
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Dong Seok LEE
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Short Communication
 - From:Nutrition Research and Practice 2025;19(1):131-142
 - CountryRepublic of Korea
 - Language:English
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		        	Abstract:
			       	
			       		
				        
				        	 BACKGROUND/OBJECTIVES:Orostachys japonicus A. Berger (O. japonicus) is a perennial herb belonging to the Crassulaceae family that has been traditionally used to treat inflammation, fever, and poisoning. Although studies on the anticancer activity of O. japonicus have been conducted, its effect on virus-induced cancers has yet to be elucidated.MATERIALS/METHODS: In the present study, we investigated the effects and mechanisms of action of the ethyl acetate fraction of O. japonicus extract (E-OJ) on the viability and apoptosis of HeLa cervical cancer cells. 
				        	
RESULTS:The effect of E-OJ on HeLa cells was compared to that of kaempferol, quercetin, and gallic acid, which are components of O. japonicus. Treatment with E-OJ induced a concentration-dependent decrease in cell viability, as confirmed by MTS assay. Pretreatment with a broad-spectrum caspase inhibitor resulted in the recovery of cell viability. Western blot analysis was conducted to determine whether the induction of apoptosis was caspasedependent. E-OJ induced apoptosis by increasing Bax/Bcl-2 ratio. Furthermore, it modulated the levels of cleaved caspase-3, -8, and -9, indicative of an impact on both the intrinsic and extrinsic pathways of apoptosis. Pretreatment with caspase inhibitors reduced caspase activity.
CONCLUSION:These results suggest that the anticancer activity of O. japonicus is mediated by caspases, resulting in a decrease in the viability of HeLa cells. 
            
