TY - JOUR
T1 - UV-induced damages eliminated by arbutin and ursolic acid in cell model of human dermal fibroblast WS-1 cells
AU - Chen, Kuan-Chou
AU - Chang, Ho-Hsing
AU - Ko, Wang Sheng
AU - Wu, Charng-Lin
AU - Chiu, Wen-Ta
AU - Hsieh, Chiu Lan
AU - Peng, Robert Y.
PY - 2009/6
Y1 - 2009/6
N2 - 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.
AB - 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.
UR - http://www.edoj.org.eg/vol005/0501/005/01.htm
M3 - Article
VL - 5
JO - Egyptian Dermatology Online Journal
JF - Egyptian Dermatology Online Journal
IS - 1
ER -