Ginsenoside Rb1 Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair

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 Rb1 in UV-induced DNA damage and apoptosis in HaCaT (keratinocyte cell line) cells, and Xpc(-) knockout mouse keratinocytes. Flow cytometry and Hoechst 33258 staining were performed in analyzing UV-induced apoptosis in keratinocytes treated with ginsenoside Rb1. The ImmunoDotBlot assay was used to detect cyclobutane pyrimidine dimers, the main sign of DNA damage. Western blot analysis was applied for analyzing Xeroderma pigmentosum-C (XPC) and excision repair cross-complementing I (ERCC I), two of the NER proteins. Ginsenoside Rb1 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 Rb1 can protect cells from apoptosis induced by UV radiation by inducing DNA repair.