Anti-melanogenesis and antigenotoxic activities of eriodictyol in murine melanoma (B16-F10) and primary human keratinocyte cells

被引:17
|
作者
Imen, Mokdad-Bzeouich [1 ,2 ]
Chaabane, Fadwa [1 ,2 ]
Nadia, Mustapha [1 ,2 ]
Soumaya, Kilani-jaziri [1 ,2 ]
Kamel, Ghedira [2 ]
Leila, Chekir-Ghedira [1 ,2 ]
机构
[1] Univ Monastir, Fac Med Dent, Lab Cellular & Mol Biol, Monastir 5000, Tunisia
[2] Univ Monastir, Fac Pharm Monastir, Unit Bioact & Nat Subst & Biotechnol UR12ES12, Monastir 5000, Tunisia
关键词
Eriodictyol; Melanogenesis; Tyrosinase activity; Comet assay; Antioxidant activity; OXIDATIVE DNA-DAMAGE; ANTIOXIDANT ACTIVITY; FLAVONOIDS; INHIBITION; APOPTOSIS; FOODS; ASSAY;
D O I
10.1016/j.lfs.2015.06.022
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Aims: The objective of this study was to examine the effect of eriodictyol on melanogenesis in cultured murine melanoma cells (B16-F10) and its antigenotoxic and antioxidant potentials on primary human keratinocyte (PHK) cells. Main methods: Anti-melanogenic effect was performed via the determination of melanin content and tyrosinase activity. Antigenotoxicity and antioxidant potentials were assessed by comet and cellular antioxidant assays, respectively. Key findings: Eriodictyol reduced melanogenesis by inhibiting the tyrosinase activity of B16-F10 cells in a dose dependant manner. Its eventual genotoxicity was investigated by evaluating its capacity to induce DNA degradation of treated cell nuclei. As no genotoxicity was detected at the different tested concentrations, its ability to protect cell DNA against hydrogen peroxide (H2O2) oxidative effect in PHK cells was investigated using the "comet assay. It appears that 50 mu M of eriodictyol solution suppressed H2O2 induced genotoxicity. In addition, this molecule revealed a significant cellular antioxidant capacity against reactive oxygen species formation in B16-F10 and PHK cells. Significance: Thus, eriodictyol could be introduced as a natural skin depigmenting agent in skin care products. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:173 / 178
页数:6
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