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Pomegranate Fruit Extract Modulates UV‐B–mediated Phosphorylation of Mitogen‐activated Protein Kinases and Activation of Nuclear Factor Kappa B in Normal Human Epidermal Keratinocytes ¶
Author(s) -
Afaq Farrukh,
Malik Arshi,
Syed Deeba,
Maes Daniel,
Matsui Mary S.,
Mukhtar Hasan
Publication year - 2005
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2005.tb01520.x
Subject(s) - photoaging , mapk/erk pathway , phosphorylation , chemistry , kinase , p38 mitogen activated protein kinases , protein kinase a , western blot , antioxidant , erythema , biochemistry , microbiology and biotechnology , biology , medicine , dermatology , immunology , gene
Excessive exposure of solar ultraviolet (UV) radiation, particularly its UV‐B component, to humans causes many adverse effects that include erythema, hyperplasia, hyperpigmentation, immunosuppression, photoaging and skin cancer. In recent years, there is increasing use of botanical agents in skin care products. Pomegranate derived from the tree Punica granatum contains anthocyanins (such as delphinidin, cyanidin and pelargonidin) and hydrolyzable tannins (such as punicalin, pedunculagin, punicalagin, gallagic and ellagic acid esters of glucose) and possesses strong antioxidant and anti‐inflammatory properties. Recently, we have shown that pomegranate fruit extract (PFE) possesses antitumor promoting effects in a mouse model of chemical carcinogenesis. To begin to establish the effect of PFE for humans in this study, we determined its effect on UV‐B–induced adverse effects in normal human epidermal keratinocytes (NHEK). We first assessed the effect of PFE on UV‐B–mediated phosphorylation of mitogen‐activated protein kinases (MAPK) pathway in NHEK. Immunoblot analysis demonstrated that the treatment of NHEK with PFE (10–40 μg/mL) for 24 h before UV‐B (40 mJ/cm 2 ) exposure dose dependently inhibited UV‐B–mediated phosphorylation of ERK1/2, JNK1/2 and p38 protein. We also observed that PFE (20 μg/mL) inhibited UV‐B–mediated phosphorylation of MAPK in a time‐dependent manner. Furthermore, in dose‐and time‐dependent studies, we evaluated the effect of PFE on UV‐B–mediated activation of nuclear factor kappa B (NF‐κB) pathway. Using Western blot analysis, we found that PFE treatment of NHEK resulted in a dose‐ and time‐dependent inhibition of UV‐B–mediated degradation and phosphorylation of IκBα and activation of IKKα. Using immunoblot analysis, enzyme‐linked immunosorbent assay and electrophoretic mobility shift assay, we found that PFE treatment to NHEK resulted in a dose‐ and time‐dependent inhibition of UV‐B–mediated nuclear translocation and phosphorylation of NF‐κB/p65 at Ser 536 . Taken together, our data shows that PFE protects against the adverse effects of UV‐B radiation by inhibiting UV‐B–induced modulations of NF‐κB and MAPK pathways and provides a molecular basis for the photochemopreventive effects of PFE.