Ginsenoside Rbl suppresses ultraviolet radiation-induced apoptosis by inducing DNA repair

Abstract

Ultraviolet (UV)-induced DNA damage is a crucial molecular trigger for sunburn cell formation and skin cancer. Nucleotide excision repair (NER) is the main mechanism in repairing UVB-induced DNA damage to mammalian cells. The purpose of this study was to investigate the functional role of ginsenoside Rbl in UV-in- duced DNA damage and apoptosis in HaCaT (keratinocyte cell line) cells, and Xpc~ knockout mouse ker- atinocytes. Flow cytometry and Hoechst 33258 staining were performed in analyzing UV-induced apoptosis in keratinocytes treated with ginsenoside Rbl. The ImmunoDotBlot assay was used to detect cyclobutane pyrimi- dine dimers, the main sign of DNA damage. Western blot analysis was applied for analyzing Xeroderma pigmen- tosum-C (XPC) and excision repair cross-complementing l (ERCCl), two of the NER proteins. Ginsenoside Rbl inhibited UV-induced apoptosis of keratinocytes and caused a notable reduction in UV-specific DNA lesions which was due to induction of DNA repair. This reduction was not observed in Xpc~ knockout keratinocytes. Ginsenoside Rb1 induced the expression of specific components of the NER complex, such as XPC and ERCC1. Our results demonstrate that ginsenoside Rbl can protect cells from apoptosis induced by UV radiation by inducing DNA repair. © 2009 Pharmaceutical Society of Japan.