Study on the Mechanism of Sinapic Acid against PC 12 Cell Injury Induced by Aβ1-42 Based on PI 3K/Akt/GSK3β Signaling Pathway
	    		
		   		
	    	
    	
    	
   		
        
        	
        		- VernacularTitle:基于PI3K/Akt/GSK3β信号通路的芥子酸抗Aβ1-42致PC12细胞损伤的机制研究
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Di XUE
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Yuchao LIU
			        		
			        		
			        		
			        			2
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Yongming JIA
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Na WANG
			        		
			        		
			        		
			        			3
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Xuewei LIU
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. School of Pharmacy,Qiqihar Medical University,Heilongjiang Qiqihar 161006,China;
			        		
			        			2. Office of Academic Research,Qiqihar Medical University,Heilongjiang Qiqihar 161006,China;
			        		
			        			3. School of Basic Medicine,Qiqihar Medical University,Heilongjiang Qiqihar 161006,China
			        		
		        		
	        		
        		 
        	
        	
        	
        		- Publication Type:Journal Article
 
        	
        	
        		- Keywords:
        			
	        			
	        				
	        				
			        		
				        		Sinapic acid;
			        		
			        		
			        		
				        		β-amyloid protein;
			        		
			        		
			        		
				        		PI3K/Akt/
			        		
			        		
	        			
        			
        		
 
        	
            
            
            	- From:
	            		
	            			China Pharmacy
	            		
	            		 2020;31(20):2519-2523
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
            	- 
		        	Abstract:
			       	
			       		
				        
				        	OBJECTIVE:To investigate the mechanism of sinapic acid (SA)against PC 12 cell injury induced by Amyloid β1-42 protein(Aβ1-42)based on PI 3K/Akt/GSK3β signaling pathway. METHODS:PC12 cells of rats were randomly divided into control group,Aβ group(Aβ1-42 2 μmol/L),Aβ+SA group(Aβ1-42 2 μmol/L+SA100 μmol/L),Aβ+SA+LY group [Aβ1-42 2 μmol/L+SA 100 μmol/L+LY294002(PI3K inhibitor )10 μmol/L],Aβ+LY group(Aβ1-42 2 μmol/L+LY294002 10 μmol/L)and LY group (LY294002 10 μmol/L). Except for control group and LY group ,the cells of other groups were replicated the damage model with Aβ1-42. After 24 hours of culture ,the morphology of cells was obsened in each group with a microscope ,and MTT assay was adopted to determine the cell viability of PC 12 cells in each group. Western blotting assay was used to detect the expression of PI 3K,p-PI3K, Akt,p-Akt,GSK3β and p-GSK3β in cells of each group. RESULTS:Compared with control group ,the number of cells decreased and some synaptic breaks disappeared in Aβ group while cell viability,ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β in Aβ group were decreased significantly(P<0.05 or P<0.01). Compared with Aβ group,the cells became round and synapses became more in Aβ+SA group while cell viability,the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β were increased significantly(P<0.05). Compared with Aβ+SA group,some synaptic breaks occurred in Aβ+SA+LY group while cell viability, the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK 3β/GSK3β were decreased significantly(P<0.05);Aβ+LY group had more cell debris,and t he cell viability was decreased ,but the difference was not significant ,and the ratio of p-PI 3K/PI3K,p-Akt/Akt and p-GSK3 β/GSK3 β had no significant change (P>0.05);  LY294002 alone had no significant effect on morphology ,cellviability and the ratio of p-PI 3K/PI3K,p-Akt/Akt or p-GSK 3β/ GSK3 β (P>0.05). CONCLUSIONS : SA may play aprotective role against PC 12 cell injury induced by A β 1-42  through activating PI 3K/Akt/GSK-3β.