Remote limb ischemic postconditioning protects focal cerebral ischemia-reperfusion injury in rats via phosphatidylinositol 3 kinase/Akt pathway
	    		
		   		
		   			
		   		
	    	
    	 
    	10.3760/cma.j.issn.1673-4165.2018.08.009
   		
        
        	
        		- VernacularTitle:肢体远隔缺血后适应通过磷脂酰肌醇3激酶/Akt通路保护大鼠局灶性脑缺血再灌注损伤
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Guofeng WANG
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Boqin LIU
			        		
			        		;
		        		
		        		
		        		
			        		Mingde GUAN
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. 266002,青岛市市立医院西院区神经内科
			        		
		        		
	        		
        		 
        	
        	
        	
        	
        		- Keywords:
        			
	        			
	        				
	        				
			        		
				        		Brain Ischemia;
			        		
			        		
			        		
				        		Reperfusion;
			        		
			        		
			        		
				        		Ischemic Postconditioning;
			        		
			        		
			        		
				        		Extremities;
			        		
			        		
			        		
				        		Neuroprotective Agents;
			        		
			        		
			        		
				        		Phosphatidylinositol 3-Kinases;
			        		
			        		
			        		
				        		Proto-Oncogene Proteins c-akt;
			        		
			        		
			        		
				        		Caspase 9;
			        		
			        		
			        		
				        		Proto-Oncogene Proteins c-bcl-2;
			        		
			        		
			        		
				        		Disease Models,Animal;
			        		
			        		
			        		
				        		Rats
			        		
			        		
	        			
        			
        		
 
        	
            
            
            	- From:
	            		
	            			International Journal of Cerebrovascular Diseases
	            		
	            		 2018;26(8):605-610
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
            	- 
		        	Abstract:
			       	
			       		
				        
				        	Objective To investigate the role of phosphatidyl inositol 3 kinase (PI3K)/Akt pathway in the protection of focal cerebral ischemia reperfusion injury in rats with limb ischemic postconditioning (LIP) by detecting the expression levels of p-Akt protein, and caspase-9 and Bcl-2 mRNAs after remote LIP. Methods Forty-two Wistar rats were randomly assigned to 3 groups: sham operation, ischemia-reperfusion (IR) and LIP groups. The middle cerebral artery ischemia-reperfusion injury model was induced by the suture method in the IR group and the LIP group. In the LIP group, three circulatory LIP ( 5 min ischemia/5 min reperfusion) in the contralateral femoral artery were performed before reperfusion 2 h after cerebral ischemia. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining. The expression of p-Akt protein was detected by immunohistochemical staining and the expression levels of cystin-9 and Bcl-2 mRNAs were detected by in situ hybridization. Results Compared with the IR group, the infarct volume in the LIP group was significantly reduced ( P<0.05). The expression levels of p-Akt protein and Bcl-2 mRNA significantly increased (all P<0.05), and the expression level of caspase-9 mRNA significantly decreased (P<0.05). Conclusions LIP can reduce the volume of cerebral infarction in focal cerebral ischemia-reperfusion injury in rats. Its mechanism may be involved in up-regulation of p-Akt protein and Bcl-2 mRNA expression and down-regulation of caspase-9 mRNA expression, suggesting that LIP can alleviate cerebral ischemia-reperfusion injury through PI3K/Akt pathway.