Differential Inhibition of UV-Induced Activation of NFκ B and AP-1 by Extracts From Black Raspberries, Strawberries, and Blueberries

Abstract

Recent studies from our laboratory have shown that the transactivation of nuclear factor κ B (NFκ B) and activator protein-1 (AP-1) plays an important mechanistic role in ultraviolet (UV)-induced skin carcinogenesis in mice. We also demonstrated that a methanol extract (ME) fraction from black raspberries (Rubus occidentalis) (RO; RO-ME) inhibits benzo[a]pyrene-7,8-diol-9,10-epoxide [B(a)PDE]–induced activation of NFκ B and AP-1 in cultured mouse epidermal cells. In the present study, we determined if RO-ME might also inhibit the induction of NFκ B and AP-1 in mouse epidermal cells exposed to mid UV radiation (UVB) and short UV radiation (UVC) and whether methanol fractions from strawberries and blueberries would also be effective. Our results showed that RO-ME inhibited UVB-induced activation of NFκ B in mouse epidermal cells in a time- and dose-dependent manner; however, the methanol fractions from strawberries and blueberries were ineffective. Interestingly, none of the fractions from all 3 berry types inhibited UVB- or UVC-induced activation of AP-1, suggesting that inhibition of UV-induced signaling pathways is specific for black raspberries and NFκ B. Cyanidin-3-rutinoside, an anthocyanin found in abundance in black raspberries and not in strawberries or high-bush blueberries, was found to contribute to the inhibition of UVB-induced activation of NFκ B. These results suggest that berries differ in their ability to influence signaling pathways leading to activation of NFκ B and AP-1 when using UV light as the inducer.

Acknowledgments and Notes

This work was supported in part by NIH/NCI Grants CA103180, CA094964, and CA112557 and NIH/NIEHS Grant ES012451.