UV-induced damages eliminated by arbutin and ursolic acid in cell model of human dermal fibroblast WS-1 cells

Kuan-Chou Chen, Ho-Hsing Chang, Wang Sheng Ko, Charng-Lin Wu, Wen-Ta Chiu, Chiu Lan Hsieh, Robert Y. Peng

Research output: Contribution to journalArticle

46 Downloads (Pure)

Abstract

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.
Original languageEnglish
JournalEgyptian Dermatology Online Journal
Volume5
Issue number1
Publication statusPublished - Jun 2009

Fingerprint

Arbutin
Fibroblasts
Matrix Metalloproteinases
Skin
Elastin
Catalase
Lipid Peroxidation
Cell Survival
Skin Aging
ursolic acid
Up-Regulation
Carcinoma

Cite this

UV-induced damages eliminated by arbutin and ursolic acid in cell model of human dermal fibroblast WS-1 cells. / Chen, Kuan-Chou; Chang, Ho-Hsing ; Ko, Wang Sheng; Wu, Charng-Lin ; Chiu, Wen-Ta; Hsieh, Chiu Lan; Peng, Robert Y.

In: Egyptian Dermatology Online Journal, Vol. 5, No. 1, 06.2009.

Research output: Contribution to journalArticle

Chen, Kuan-Chou ; Chang, Ho-Hsing ; Ko, Wang Sheng ; Wu, Charng-Lin ; Chiu, Wen-Ta ; Hsieh, Chiu Lan ; Peng, Robert Y. / UV-induced damages eliminated by arbutin and ursolic acid in cell model of human dermal fibroblast WS-1 cells. In: Egyptian Dermatology Online Journal. 2009 ; Vol. 5, No. 1.
@article{f077bfd1b19943d6ac135d47ef785b9f,
title = "UV-induced damages eliminated by arbutin and ursolic acid in cell model of human dermal fibroblast WS-1 cells",
abstract = "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.",
author = "Kuan-Chou Chen and Ho-Hsing Chang and Ko, {Wang Sheng} and Charng-Lin Wu and Wen-Ta Chiu and Hsieh, {Chiu Lan} and Peng, {Robert Y.}",
year = "2009",
month = "6",
language = "English",
volume = "5",
journal = "Egyptian Dermatology Online Journal",
number = "1",

}

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 -