The effects of epigallocatechin-3-gallate on extracellular matrix metabolism.
BACKGROUND
Anti-oxidants have attracted a lot of interest on account of their function to protect the skin from oxidative stress by ultraviolet (UV) radiation.


OBJECTIVE
This study examined the effects of epigallocatechin-3-gallate (EGCG), which is a green tea extract, on the extracellular matrix (ECM) changes induced by UV radiation and showed the comparative results with retinoic acid (RA).


METHODS
The ECM metabolism is tightly controlled by the collagen degrading matrix metalloprotienases (MMPs) and their tissue inhibitors (TIMPs). Therefore, the expression of MMPs and TIMP-1 was investigated to evaluate the effects of EGCG and RA. Artificial skin was made using three-dimensionally cultured keratinocytes on a collagen matrix populated with fibroblasts. EGCG and RA were added into the medium of the fibroblasts and keratinocytes culture and also applied topically on artificial skins prior to UVA irradiation. The MMPs and TIMP-1 expression levels were measured using Western blot and a zymogram.


RESULTS
EGCG, like RA, decreased the level of MMPs production and increased TIMP-1 expression level. However, EGCG suppressed the activities of the gelatinases and augmented the expressions of the TIMP-1 more than RA did. RA decreased the MMP-1 and MMP-3 expression levels to a greater extent than EGCG. ECM alterations as a result of UVA appeared to be prevented more effectively using the EGCG treatment.


CONCLUSIONS
EGCG can reverse the ECM degradation induced by UV even with a topical application of a practical-use concentration. In particular, EGCG proved to be much more effective in ROS-related conditions, such as UVA exposure.
Lee
Jong Hee
JH
Department of Dermatology, Seoul National University College of Medicine, Institute of Dermatological Science, 28 Yongon-Dong, Chongno-Gu, Seoul 110-744, Republic of Korea.
Chung
Jin Ho
JH
Cho
Kwang Hyun
KH
D000975:Antioxidants / Q000494:pharmacology*; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002478:Cells, Cultured; D020405:Dermis / Q000166:cytology; D000078404:Epidermal Cells; D005109:Extracellular Matrix / Q000378:metabolism*; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D015603:Keratinocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D007641:Keratolytic Agents / Q000494:pharmacology; D020782:Matrix Metalloproteinases / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000528:radiation effects; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D014212:Tretinoin / Q000494:pharmacology; D014466:Ultraviolet Rays
D000975:Antioxidants; D007641:Keratolytic Agents; D019715:Tissue Inhibitor of Metalloproteinase-1; D014212:Tretinoin; D002392:Catechin; C045651:epigallocatechin gallate; D020782:Matrix Metalloproteinases