Abstract
Ginsenosides, the major active ingredients of ginseng, show a variety of biomedical efficacies such as antiaging and antioxidation. Here, we investigate the protective activity of the ginsenoside F1, an enzymatically modified derivative of ginsenoside Rg1, against ultraviolet-B-induced damage in human HaCaT keratinocytes. Ginsenoside F1 significantly reduced ultraviolet-B-induced cell death and protected HaCaT cells from apoptosis caused by ultraviolet B irradiation. Furthermore, ginsenoside F1 prevented ultraviolet-B-induced cleavage of poly(ADP-ribose) polymerase in HaCaT cells. In search of the molecular mechanism responsible for the antiapoptotic effect of ginsenoside F1, we find that protection from ultraviolet-B-induced apoptosis is tightly correlated with ginsenoside-F1-mediated inhibition of ultraviolet-B-induced downregulation of Bcl-2 and Brn-3a expression.
MeSH terms
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Apoptosis / drug effects*
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Apoptosis / radiation effects*
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Cell Line
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DNA-Binding Proteins / metabolism
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Dose-Response Relationship, Drug
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Down-Regulation / drug effects
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Down-Regulation / radiation effects
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Epidermal Cells
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Gene Expression / drug effects
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Gene Expression / radiation effects
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Ginsenosides / pharmacology*
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Humans
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Keratinocytes / cytology
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Keratinocytes / drug effects*
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Keratinocytes / radiation effects*
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Promoter Regions, Genetic / physiology
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Promoter Regions, Genetic / radiation effects
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Proto-Oncogene Proteins c-bcl-2 / genetics*
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Transcription Factor Brn-3
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Transcription Factor Brn-3A
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Transcription Factors / metabolism
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Transcription, Genetic / drug effects
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Transcription, Genetic / radiation effects
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Ultraviolet Rays / adverse effects
Substances
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DNA-Binding Proteins
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Ginsenosides
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POU4F1 protein, human
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Proto-Oncogene Proteins c-bcl-2
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Transcription Factor Brn-3
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Transcription Factor Brn-3A
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Transcription Factors
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ginsenoside F1