Effect of Nobiletin on LPS-Induced Inflammatory Injury of Mesangium Cells by Regulating AMPK/NLRP3 Signaling Pathway
	    		
		   		
		   			
		   		
	    	
    	 
    	10.19378/j.issn.1003-9783.2024.02.009
   		
        
        	
        		- VernacularTitle:川陈皮素调节AMPK/NLRP3信号通路对脂多糖诱导的肾小球系膜细胞炎性损伤的影响
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Dan LUO
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Yan WANG
			        		
			        		;
		        		
		        		
		        		
			        		Xu DING
			        		
			        		;
		        		
		        		
		        		
			        		Yao HU
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. 成都大学附属医院血液净化中心,四川 成都 610081
			        		
		        		
	        		
        		 
        	
        	
        	
        	
        		- Keywords:
        			
	        			
	        				
	        				
			        		
				        		nobiletin;
			        		
			        		
			        		
				        		AMP-activated protein kinase(AMPK)/NOD-like receptor protein 3(NLRP3)signaling pathway;
			        		
			        		
			        		
				        		lipopolysaccharide;
			        		
			        		
			        		
				        		mesangium cells;
			        		
			        		
			        		
				        		HBZY-1;
			        		
			        		
			        		
				        		inflammatory injury
			        		
			        		
	        			
        			
        		
 
        	
            
            
            	- From:
	            		
	            			Traditional Chinese Drug Research & Clinical Pharmacology
	            		
	            		 2024;35(2):224-229
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
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		        	Abstract:
			       	
			       		
				        
				        	Objective To investigate the effect of nobiletin(Nb)on lipopolysaccharide(LPS)-induced inflammatory injury of mesangium cells(HBZY-1)by regulating AMP-activated protein kinase(AMPK)/NOD-like receptor protein 3(NLRP3)signaling pathway.Methods HBZY-1 cells were separated into 5 groups:normal control(NC)group,LPS group(100 ng·mL-1 LPS),and Nb group(100 ng·mL-1 LPS+40 μmol·L-1 Nb),Rapamycin(Rap,AMPK/NLRP3 signaling pathway inhibitor)group[100 ng·mL-1 LPS+0.5 μmol·L-1 Rap],and Nb+Rap group(100 ng·mL-1 LPS+40 μmol·L-1 Nb+0.5 μmol·L-1 Rap).MTT was applied to detect the cytotoxicity and proliferation of HBZY-1 cells.ELISA was applied to detect the contents of interleukin(IL)-1β,IL-6,tumor necrosis factor-α(TNF-α),catalase(CAT),superoxide dismutase(SOD),and glutathione(GSH)in HBZY-1 cells.Flow cytometry was used to detect cell apoptosis.Western Blot was applied to detect the protein levels of AMPK/NLRP3 signaling pathway.Results Compared with the NC group,the levels of CAT,SOD,GSH,cell OD value,and the level of AMPK protein in the LPS group were significantly reduced(P<0.05).The apoptosis rate,contents of IL-1β,IL-6,TNF-α,and the level of NLRP3 protein were significantly increased(P<0.05).Compared with the LPS group,the levels of CAT,SOD,GSH,OD value,and the level of AMPK protein in the Nb group were significantly increased(P<0.05).The apoptosis rate,contents of IL-1β,IL-6,TNF-α,and the level of NLRP3 protein were significantly decreased(P<0.05),while the above indicators in the Rap group showed an opposite trend to the Nb group(P<0.05).Compared with the Nb group,the above indicators in the Nb+Rap group also showed an opposite trend to the Nb group(P<0.05).Conclusion Nb may alleviate LPS-induced inflammatory injury to MC cells by up-regulating the AMPK/NLRP3 signaling pathway.But down-regulation of the AMPK/NLRP3 signaling pathway may eliminate the improvement effect of Nb on LPS-induced inflammatory injury in MC cells.