Naringenin protects human keratinocytes against UVB-induced damage: Role of cellular apoptosis and DNA repair

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DNA damage and apoptosis caused by solar ultraviolet (UV) radiation are considered the main etiologic factors contributing to the development of skin cancer and photoaging. The use of antioxidants has been suggested as an effective chemoprotective strategy against UV-induced skin damage. Herein, we have investigated the potential chemopreventive effect of naringenin (NG), a naturally occurring citrus flavonoid with antioxidant properties, on UVB-induced damage in human keratinocyte, HaCat, cell line. Cells were pretreated with NG 30 min prior to UV irradiation at doses of 25, 50, or 100 mJ/cm². Colony-forming efficiency, malondialdehyde (MDA) production, cellular apoptosis, and genomic DNA repair were measured. A significantly higher number of colonies were noted following the treatment with different concentrations of NG compared to UVB treated cells. This protective effect was also supported by the potential of NG to protect cells from UVB induced apoptosis, as observed by the disappearance of a 180 base pair ladders and the sub-G1 peak using agarose gel electrophoresis and flow cytometric analysis. Treatment of keratinocytes with NG resulted in a significant reduction of MDA level in NG-treated cells compared to controls, indicating that NG prevented the UVB-induced lipid peroxidation. Moreover, the removal of cyclobutane pyrimidine dimers (CPD) from the genome was enhanced in NG treated cells, indicating an increased efficiency of nucleotide excision repair. These results suggest that NG is a promising antioxidant natural flavonoid capable to protect human keratinocytes from UVB-induced damage partly through inhibition of apoptosis and enhancement of CPD removal.

(Supported by NIH grants ES2388, ES12991 and CA93413).