PubMed · 2004 · 21 citations · 0 references
MedicineDermatologyMolecular BiologyCell SignalingSignal TransductionTranscriptional RegulationBiological Effects Of RadiationCellular Radiation ResponseSun ProtectionTissue Responses To RadiationUltraviolet Radiation BiologyUltraviolet Radiation ProtectionDermatological PhotoprotectionIonizing IrradiationProtein Expression LevelsUltraviolet IrradiationUltraviolet Radiation DamageUva ProtectionUvb ProtectionWestern Blot Analysis
BACKGROUND: It 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. METHODS: Transcription 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). RESULTS: EGCG 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). CONCLUSION: EGCG 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.