Exogenous spermine contributes to prevent apoptosis in the rat hearts and cardiomyocytes
	    		
		   		
	    	
    	
    	
   		
        
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Can WEI
			        		
			        		;
		        		
		        		
		        		
			        		Yuehong WANG
			        		
			        		;
		        		
		        		
		        		
			        		Meixiu LI
			        		
			        		;
		        		
		        		
		        		
			        		Hongzhu LI
			        		
			        		;
		        		
		        		
		        		
			        		Hongjiang SHAO
			        		
			        		;
		        		
		        		
		        		
			        		Changqing XU
			        		
			        		
		        		
		        		
		        		
		        		
		        		
			        		
			        		
		        		
	        		
        		 
        	
        	
        	
        		- Publication Type:Journal Article
 
        	
        	
            
            
            	- From:
	            		
	            			Chinese Journal of Pathophysiology
	            		
	            		 2016;32(8):1517-1517
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
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		        	Abstract:
			       	
			       		
				        
				        	AIM:To investigate the relationship between polyamine metabolism and hypoxia /ischemia ( H/I)-induced cell apoptosis and to determine the mechanisms by which exogenous spermine protects cell apoptosis against AMI in rats .METHOD:The left anterior de-scending coronary artery ( LAD) of the Wistar rats were ligated , and neonatal rat cardiomyocytes were placed under hypoxic conditions for 24 h to establish the model of AMI (or H/I).Exogenous spermine was administered by intraperitoneal injection (2.5 mg/kg daily for 7 days) in vitro and subjected to the cell medium at 5μmol/L as a pre-treatment therapy.RESULTS:AMI (or H/I) induced an increase in polyamine catabolized enzyme SSAT and a decrease in polyamine biosynthesis enzyme ODC , which result in endogenous spermine and spermidine decrease and putrescine increase .At the same time, AMI ( or H/I) lowered cardiac function , increased cTnI and CK-MB concentrations , aggravated myocardial infarct size , cardiomyocyte damage and apoptosis , raised ROS generation , increased the expression of cleaved caspase-3, cleaved caspase-9 and endoplasmic reticulum stress (ERS)-related proteins, promoted the release of cytochrome C and mPTP opening , down-regulated Bcl-2 expression and the phosphorylation of ERK 1/2, PI3K, Akt and GSK-3β, and activated PERK and eIF 2αphosphorylation .Spermine pre-treatment reversed the above-motioned changes .CONCLUSION:AMI ( or H/I ) could induce cardiomyocyte apoptosis and polyamine metabolism disorder .Exogenous spermine attenuates cardiac injury through scavenging the ROS and inhibiting mPTP opening and ERS injury .These findings provide a novel target for the prevention of apoptosis in the setting of AMI .