Xinfeng Capsule alleviates interleukin-1β-induced chondrocyte inflammation and extracellular matrix degradation by regulating the miR-502-5p/TRAF2/NF-κB axis
	    		
		   		
		   			
		   		
	    	
    	 
    	10.12122/j.issn.1673-4254.2024.01.13
   		
        
        	
        		- VernacularTitle:新风胶囊抑制软骨细胞炎症和细胞外基质降解:基于调控miR-502-5p/TRAF2/NF-κB轴
 
        	
        	
        	
        		- Author:
	        		
		        		
		        		
			        		Qiao ZHOU
			        		
			        		
			        		
			        			1
			        			
			        		
			        		
			        		
			        		
			        		;
		        		
		        		
		        		
			        		Jian LIU
			        		
			        		;
		        		
		        		
		        		
			        		Lei WAN
			        		
			        		;
		        		
		        		
		        		
			        		Yan ZHU
			        		
			        		;
		        		
		        		
		        		
			        		Yajun QI
			        		
			        		;
		        		
		        		
		        		
			        		Yuedi HU
			        		
			        		
		        		
		        		
		        		
		        		
		        			
			        		
			        		Author Information
			        		
		        		
		        		
			        		
			        		
			        			1. 安徽中医药大学第二附属医院,安徽 合肥 230061;安徽中医药大学,安徽 合肥 230012
			        		
		        		
	        		
        		 
        	
        	
        	
        	
        		- Keywords:
        			
	        			
	        				
	        				
			        		
				        		miR-502-5p;
			        		
			        		
			        		
				        		osteoarthritis;
			        		
			        		
			        		
				        		Xinfeng Capsule;
			        		
			        		
			        		
				        		inflammation;
			        		
			        		
			        		
				        		extracellular matrix
			        		
			        		
	        			
        			
        		
 
        	
            
            
            	- From:
	            		
	            			Journal of Southern Medical University
	            		
	            		 2024;44(1):108-118
	            	
            	
 
            
            
            	- CountryChina
 
            
            
            	- Language:Chinese
 
            
            
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		        	Abstract:
			       	
			       		
				        
				        	Objective To investigate the mechanism that mediates the inhibitory effect of Xinfeng Capsule(XFC)on interleukin(IL)-1β-induced impairment of chondrocytes.Methods XFC-medicated serum was collected from SD rats with XFC gavage,and its optimal concentration for chondrocyte treatment was determined using Cell Counting Kit-8 assay and flow cytometry.Dual luciferase reporter analysis was performed to analyze the targeting relationship between miR-502-5p and TRAF2.In cultured human chondrocytes induced with IL-1β,the effects of transfection with miR-502-5p inhibitor and XFC-medicated serum,alone or in combination,on expression levels of IL-1β,tumor necrosis factor-α(TNF-α),IL-4,and IL-10 were examined with ELISA,and the changes in the expressions of collagen type Ⅱ alpha 1(COL2A1),matrix metalloproteinase 13(MMP13),adisintegrin and metalloproteinase with thrombospondin motifs 5(ADAMTS5),and miR-502-5p/TRAF2/NF-κB axis gene expression were detected using RT-qPCR,Western blotting,and immunofluorescence assay.Results In cultured human chondrocytes,treatment with IL-1β significantly decreased the cell viability,increased cell apoptosis rate,lowered miR-502-5p,IL-4,IL-10,and COL2A1 expressions,and enhanced IL-1β,TNF-α,ADAMTS5,MMP13,TRAF2,and NF-κB p65 expressions(P<0.05),and these changes were significantly improved by treatment with XFC-medicated serum at the optimal concentration of 20%(P<0.05).Transfection of the chondrocytes with miR-502-5p inhibitor resulted in elevated expressions of IL-1β,TNF-α,ADAMTS5,MMP13,TRAF2,and NF-κB p65 and lowered expressions of miR-502-5p,IL-4,IL-10,and COL2A1,and XFC-medicated serum obviously reversed the effects of miR-502-5p inhibitor.Conclusion XFC can inhibit IL-1β-induced inflammatory response and ECM degradation in cultured human chondrocytes possibly by regulating the miR-502-5p/TRAF2/NF-κB axis.