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* Department of Dermatology, Seoul National University College of Medicine, Laboratory of Cutaneous Aging Research, Clinical Research Institutes, Seoul National University Hospital, and Institute of Dermatological Science, Seoul National University, Seoul, Korea
Department of Dermatology, Seoul National University Boramae Hospital, Seoul, Korea
Published, JLR Papers in Press, February 7, 2006.
1 To whom correspondence should be addressed. e-mail: jhchung{at}snu.ac.kr
Skin aging can be attributed to photoaging (extrinsic) and chronological (intrinsic) aging. Photoaging and intrinsic aging are induced by damage to human skin attributable to repeated exposure to ultraviolet (UV) irradiation and to the passage of time, respectively. In our previous report, eicosapentaenoic acid (EPA) was found to inhibit UV-induced matrix metalloproteinase-1 (MMP-1) expression in human dermal fibroblasts. Therefore, we investigated the effects of EPA on UV-induced skin damage and intrinsic aging by applying EPA topically to young and aged human skin, respectively. By immunohistochemical analysis and Western blotting, we found that topical application of EPA reduced UV-induced epidermal thickening and inhibited collagen decrease induced by UV light. It was also found that EPA attenuated UV-induced MMP-1 and MMP-9 expression by inhibiting UV-induced c-Jun phosphorylation, which is closely related to UV-induced activator protein-1 activation, and by inhibiting JNK and p38 activation. EPA also inhibited UV-induced cyclooxygenase-2 (COX-2) expression without altering COX-1 expression. Moreover, it was found that EPA increased collagen and elastic fibers (tropoelastin and fibrillin-1) expression by increasing transformin growth factor-ß expression in aged human skin. Together, these results demonstrate that topical EPA has potential as an anti-skin-aging agent.
Supplementary key words polyunsaturated fatty acid intrinsic aging photoaging ultraviolet irradiation
Abbreviations: AA, arachidonic acid; AP-1, activator protein-1; COX-2, cyclooxygenase-2; DHA, docosahexaenoic acid; ECM, extracellular matrix; EPA, eicosapentaenoic acid; MAPK, mitogen-activated protein kinase; MED, minimal erythma dose; MMP, matrix metalloproteinase; PG, prostaglandin; TGF-ß, transforming growth factor-ß; UV, ultraviolet
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