Effects of α-Santalol on Proapoptotic Caspases and p53 Expression in UVB Irradiated Mouse Skin

Abstract

Background: Cancer chemoprevention by naturally occurring agents, especially phytochemicals, minerals and vitamins has shown promising results against various malignancies in a number of studies both under in vitro and in vivo conditions. One such phytochemical, α-santalol, a major component of sandalwood oil, is effective in preventing skin cancer in both chemically and UVB-induced skin cancer development in CD-1, SENCAR and SKH-1 mice; however, the mechanism of its efficacy is not fully understood. The objective of the present investigation was to study the effects of α-santalol on apoptosis proteins and p53 in UVB-induced skin tumor development in SKH-1 mice to elucidate the mechanism of action. Materials and Methods: Female SKH-1 mice were divided into two groups: Group 1, which served as control received topical application of acetone (0.1 ml) one hour before UVB treatment; Group 2 received α-santalol (0.1 ml, 5% w/v in acetone, topical) one hour prior to UVB treatment. UVB-induced promotion was continued for 30 weeks. Results: Pretreatment with α-santalol one hour prior to UVB exposure significantly (p<0.05) reduced tumor incidence and multiplicity, and resulted in a significant (p<0.05) increase in apoptosis proteins, caspase-3 and -8 levels and tumor suppressor protein, p53. Conclusion: These results suggest that α-santalol prevents skin cancer development by inducing proapoptotic proteins via an extrinsic pathway and increasing p53.