Role of Salvia miltiorrhiza for Modulation of Th2-derived Cytokines in the Resolution of Inflammation.
	    		
		   		
		   			
		   		
	    	
    	- Author:
	        		
		        		
		        		
			        		Sunhee MOON
			        		
			        		
			        		
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			        		Seulmee SHIN
			        		
			        		;
		        		
		        		
		        		
			        		Seulah KIM
			        		
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			        		Hee Eun OH
			        		
			        		;
		        		
		        		
		        		
			        		Shinha HAN
			        		
			        		;
		        		
		        		
		        		
			        		Seungjeong LEE
			        		
			        		;
		        		
		        		
		        		
			        		Kyungjae KIM
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Original Article
 - Keywords: Salvia miltiorrhiza; Pro-inflammatory cytokines; Chemokine; Th2 cytokine
 - MeSH: Chemokine CCL5; Chemokines; Cytokines; Down-Regulation; Edema; Ethanol; Inflammation; Interleukin 1 Receptor Antagonist Protein; Interleukin-10; Interleukin-4; Interleukin-6; Salvia; Salvia miltiorrhiza; Transforming Growth Factor beta; Tumor Necrosis Factor-alpha
 - From:Immune Network 2011;11(5):288-298
 - CountryRepublic of Korea
 - Language:English
 - Abstract: BACKGROUND: Salvia miltiorrhiza (SM) has been used to treat inflammatory diseases including edema and arthritis; however, the anti-inflammatory mechanism of SM action remains unresolved. METHODS: The effects of an ethanol extract of SM (ESM) on pro-inflammatory cytokines such as TNF-alpha, IL-1beta, IL-6, and NO, on anti-inflammatory cytokines including IL-4, IL-10, TGF-beta, and IL-1Ra have been studied in an attempt to elucidate the anti-inflammatory mechanism in murine macrophages. RESULTS: ESM inhibited the production of pro-inflammatory cytokines via down-regulation of gene and protein expression whereas it increased the anti-inflammatory cytokines. Furthermore, ESM inhibited the expression of the chemokines, RANTES and CX3CL1, as well as of inflammatory mediators such as TLR-4 and 11beta-HSD1. CONCLUSION: These results indicated that the regulatory effects of ESM may be mediated though the suppression of pro-inflammatory cytokines as well as the induction of anti-inflammatory cytokines. Consequently, we speculate that ESM has therapeutic potential for inflammation-associated disorders.
 
            