Effects of (-)-epigallocatechin-3-gallate on expression of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in fibroblasts irradiated with ultraviolet A.
- Author:
	        		
		        		
		        		
			        		Xiu-zu SONG
			        		
			        		
			        		
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			        		Ji-ping XIA
			        		
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			        		Zhi-gang BI
			        		
			        		
		        		
		        		
		        		
			        		
			        		Author Information
			        		
 - Publication Type:Journal Article
 - MeSH: Catechin; analogs & derivatives; pharmacology; Cells, Cultured; Fibroblasts; metabolism; radiation effects; Gene Expression Regulation; drug effects; Humans; Matrix Metalloproteinase 1; biosynthesis; genetics; Proto-Oncogene Proteins c-jun; analysis; RNA, Messenger; analysis; Radiation-Protective Agents; pharmacology; Reverse Transcriptase Polymerase Chain Reaction; Tissue Inhibitor of Metalloproteinase-1; biosynthesis; genetics; Ultraviolet Rays
 - From: Chinese Medical Journal 2004;117(12):1838-1841
 - CountryChina
 - Language:English
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		        	Abstract:
			       	
			       		
				        
				        	
BACKGROUNDIt is known that ultraviolet irradiation can affect cellular function through a number of signaling pathways. (-)-epigallocatechin-3-gallate (EGCG) is the major effective component in green tea and can offer protection from ultraviolet-induced damage. In this study, we investigated the protective mechanism of EGCG on human dermal fibroblasts damaged by ultraviolet A (UVA) in vitro.
METHODSTranscription factor Jun protein levels were measured by Western blot. Matrix metalloproteinase 1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA were studied by reverse transcription-polymerase chain reaction (RT-PCR) analysis in conjunction with computer-assisted image analysis. MMP-1 and TIMP-1 proteins were quantified by enzyme-linked immunosorbent assay (ELISA).
RESULTSEGCG decreased transcription activity of Jun protein after induction by UVA. Both the mRNA and protein levels of MMP-1 were increased by UVA irradiation, while no significant changes were observed in TIMP-1 levels. The ratio of MMP-1 to TIMP-1 showed statistically significant differences compared with the control. EGCG decreased the ratio of MMP-1 to TIMP-1 by inhibiting UVA-induced MMP-1 expression (P < 0.05).
CONCLUSIONEGCG can protect human fibroblasts against UVA damage by downregulating the transcription activity of Jun protein and the expression of MMP-1. The ratio of MMP-1 to TIMP-1, rather than the levels of MMP-1 or TIMP-1 alone, may play a significant role in human skin photodamage.
 
            