title: Ginsenoside F1 protects human HaCaT keratinocytes from ultraviolet-B-induced apoptosis by maintaining constant levels of Bcl-2.
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.
authors.affiliation: R & D Center, AmorePacific Corporation, 314-1 Bora-ri, Giheung-eup, Yongin-si, Kyeonggi-do 449 729, Korea.
authors.forename: Enn Hee
authors.initials: EH
authors.lastname: Lee
authors.forename: Si Young
authors.initials: SY
authors.lastname: Cho
authors.forename: Su Jong
authors.initials: SJ
authors.lastname: Kim
authors.forename: Eui Seok
authors.initials: ES
authors.lastname: Shin
authors.forename: Hui Kyoung
authors.initials: HK
authors.lastname: Chang
authors.forename: Duck Hee
authors.initials: DH
authors.lastname: Kim
authors.forename: Myeong Hoon
authors.initials: MH
authors.lastname: Yeom
authors.forename: Kwang Sik
authors.initials: KS
authors.lastname: Woe
authors.forename: Jinseon
authors.initials: J
authors.lastname: Lee
authors.forename: Young Chul
authors.initials: YC
authors.lastname: Sim
authors.forename: Tae Ryong
authors.initials: TR
authors.lastname: Lee
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects*; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects / Q000528:radiation effects; D000078404:Epidermal Cells; D015870:Gene Expression / Q000187:drug effects / Q000528:radiation effects; D036145:Ginsenosides / Q000494:pharmacology*; D006801:Humans; D015603:Keratinocytes / Q000166:cytology / Q000187:drug effects* / Q000528:radiation effects*; D011401:Promoter Regions, Genetic / Q000502:physiology / Q000528:radiation effects; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics*; D050818:Transcription Factor Brn-3; D050819:Transcription Factor Brn-3A; D014157:Transcription Factors / Q000378:metabolism; D014158:Transcription, Genetic / Q000187:drug effects / Q000528:radiation effects; D014466:Ultraviolet Rays / Q000009:adverse effects
chemical_list: D004268:DNA-Binding Proteins; D036145:Ginsenosides; C494188:POU4F1 protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D050818:Transcription Factor Brn-3; D050819:Transcription Factor Brn-3A; D014157:Transcription Factors; C055327:ginsenoside F1