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KMID : 1023120130110010093
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Korean Journal of Aesthetic Society
2013 Volume.11 No. 1 p.93 ~ p.102
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Gene Expression Profiling in Protection Mechanism of Silibinin Against Damage to Human Dermal Fibroblasts Caused by UVB
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Yoon Yeong-Min
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Abstract
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Cellular aging can be divided into intrinsic or extrinsic aging. Extrinsic aging is caused by various external factors which include ultraviolet (UV). UV irradiation has various biological effects on skin, such as erythema, sunburn, skin cancer and photoaging. Silibinin is the major active constituent of silymarin that is a mixture of flavonolignans isolated from milk thistle seeds. Silibinin has effects of anti-cancer, anti-oxidant, anti-apoptotic and anti-inflammatory. In this study, we investigated the protection effect of silibinin against damage to human dermal fibroblasts (HDFs) caused by UVB. We confirmed the effects of silibinin using cell viability, Western blotting, DNA microarray and quantitative real-time PCR (qRT-PCR). Silibinin at concentrations of 1 ? 10 μM did not affect cell viability. When UVB-induced HDFs were pretreated silibinin, cell viability of HDFs increased in a dose-dependent manner. Also, silibinin reduced nuclear accumulation of p53, a homotetrameric transcription factor, and expression of p21 in irradiation of HDFs with UVB. We also analyzed gene expression level using DNA microarrays and showed that 66 mRNAs were differentially expressed in UVB- induced HDFs with pretreatment with silibinin. Among them, 34 genes were up-regulated and 32 genes were down- regulated. Silibinin regulated the expression of HMOX1, E2F7, GADD45A and TP53I3, which are regulate anti-oxidation, apoptosis, DNA repair and cell cycle arrest. Differential expression of these genes was confirmed using qRTPCR. mRNA expression levels of HMOX1 and E2F7 were increased in UVB-induced HDFs with pre-treatment with silibinin. In contrast, expression of GADD45A and TP53I3 mRNAs was decreased in treated cells. These findings suggest that silibinin might be used as a natural ingredient for the protection of UVB-induced skin damage.
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KEYWORD
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UVB, HDFs, Silibinin, p53, Gene expression profiling
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