Objectives: UV irradiation may cause dermal ageing and carcinoma. The molecular action mechanism of such an effect and the methods for prevention are still lacking. Materials and Methods: UVA (320-400 nm) plus UVB (290-320 nm) (hereafter denoted as UVAB) was used to induce skin damages in human fibroblast WS1 (hfWS1) cells. The parameters evaluated included the cell viability, expressions of relevant enzymes including MMP-1, MMP-2, catalase, and LDH; some biochemical indices such as elastin content and lipid peroxidation. Arbutin (AB) and ursolic acid (UA) were used to evaluate whether they could show any protective effect. Results: UVAB inhibited the viability of hfWS1 cells, leading to a lowered elastin biosynthesis, enhanced release of LDH, and up-regulation of MMP-1, MMP-2 and catalase. Moreover it accelerated lipid peroxidation. In this regard, AB and UA behaved differently. On treatment with AB and/or UA, the cell viability was effectively protected by AB at dose <10 M and by UA at 1 M. In contrast, apparent cytotoxicity was shown by UA at 10 M. Although the extracellular elastin levels were recovered, yet were insignificant. At a dose of 100 M, the lipid peroxidation was effectively suppressed by UA but not by AB. At 0.1 M, both AB and UA effectively suppressed the LDH release to the control level. Molecular action mechanism revealed both AB and UA at 1-2 M significantly down-regulated the expressions of catalase, MMP-2 but not MMP-1.
|Egyptian Dermatology Online Journal
|Published - Jun 2009