Journal
EXPERIMENTAL GERONTOLOGY
Volume 61, Issue -, Pages 147-155Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2014.12.008
Keywords
18 beta-Glycyrrhetinic acid; Skin photoaging; Ultraviolet; Anti-inflammation; Anti-oxidant; Matrix metalloproteinases
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Funding
- program for scientific research start-up funds of Guangdong Ocean University
- College students' innovation and entrepreneurship training plan of Guangdong Province [201410572091]
- special funds from the central finance of China in support of the development of local Colleges and University [276(2014)]
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It has been confirmed that repeated exposure of skin to ultraviolet (UV) radiation results in cutaneous oxidative stress and inflammation, which act in concert to cause premature skin aging, well known as photoaging. 18 beta-Glycyrrhetinic acid (GA), widely used to treat various tissue inflammations, is the main active component of licorice root, and has also been shown to possess favorable anti-oxidative property and modulating immunity function. In the present study, we investigated the potential protective effect of GA on UV-induced skin photoaging in a mousemodel. During the experimental period of ten consecutive weeks, the dorsal depilated skin of mice was treated with topical GA for 2 hours prior to UV irradiation. The results showed that GA pretreatment significantly alleviated the macroscopic and histopathological damages in mice skin caused by UV. Meanwhile, the data also indicated that GA markedly up-regulated the activities of the antioxidant enzymes (SOD, GSH-Px), and increased the content of skin collagen, while obviously decreased malonaldehyde level and inhibited high expressions of matrix metalloproteinase-1 (MMP-1) and -3 (MMP-3), as well as down-regulated the expression of inflammatory cytokines such as IL-6, TNF-alpha and IL-10. Taken together, these findings amply demonstrate that GA observably attenuates UV-induced skin photoaging mainly by virtue of its antioxidative and anti-inflammatory properties, as well as regulating the abnormal expression of MMP-1 and MMP-3. (C) 2014 Elsevier Inc. All rights reserved.
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