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Lonicera caerulea and Vaccinium myrtillus fruit polyphenols protect HaCaT keratinocytes against UVB-induced phototoxic stress and DNA damage

Alena SvobodováCorresponding Author Informationemail address, Adéla Zdařilová, Jitka Vostálová

Received 17 April 2009; received in revised form 10 August 2009; accepted 19 August 2009. published online 12 July 2010.
Corrected Proof

Abstract 

Background

Sunlight is a very potent environmental factor in skin pathogenesis and can induce skin cancer. UVB irradiation is known to cause oxidative stress, inflammation and especially DNA damage. Topical application of agents with UV absorbing, antioxidant and anti-inflammatory activities is a successful strategy in the protection of the skin against UV-caused damage.

Objective

To examine the ability of the phenolic fraction of Lonicera caerulea and Vaccinum myrtillus fruits to moderate UVB-induced damage.

Methods

HaCaT keratinocytes, a well-established in vitro system for investigations on UV radiation induced cell damage, were used to assess the effects of pre- and post-treatment with L. caerulea (LCE) and V. myrtillus (VME) phenolic fractions (5–50mg/l) on keratinocyte damage induced by a solar simulator (295–315nm).

Results

In this study, a model of UVB-induced damage to HaCaT was established. LCE and VME efficiently reduced the extent of DNA breakage (especially at concentrations of 25 and 10mg/l) together with caspase-3 and -9 activity and DNA laddering induced by UVB (100 or 200mJ/cm2). LCE and VME significantly decreased RONS generation and partially diminished IL-6 expression. LCE pre-treatment also prevented keratinocytes proliferation.

Conclusion

The results suggest that the phenolic fraction of L. caerulea and V. myrtillus fruits suppress UVB-caused injury to keratinocytes. These results now need to be demonstrated in vivo.

Department of Medical Chemistry and Biochemistry, Faculty of Medicine and Dentistry, Palacký University, Hněvotínská 3, 775 15 Olomouc, Czech Republic

Corresponding Author InformationCorresponding author. Tel.: +420 585632314; fax: +420 585632302.

PII: S0923-1811(09)00258-8

doi:10.1016/j.jdermsci.2009.08.004