This paper is part of the Special Issue in Commemoration of the 70th birthday of Dr. David R. Bickers.
Pomegranate Fruit Extract Inhibits UVB-induced Inflammation and Proliferation by Modulating NF-κB and MAPK Signaling Pathways in Mouse Skin†
Article first published online: 13 JAN 2012
© 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The American Society of Photobiology
Photochemistry and Photobiology
Volume 88, Issue 5, pages 1126–1134, September/October 2012
How to Cite
Khan, N., Syed, D. N., Pal, H. C., Mukhtar, H. and Afaq, F. (2012), Pomegranate Fruit Extract Inhibits UVB-induced Inflammation and Proliferation by Modulating NF-κB and MAPK Signaling Pathways in Mouse Skin. Photochemistry and Photobiology, 88: 1126–1134. doi: 10.1111/j.1751-1097.2011.01063.x
- Issue published online: 5 SEP 2012
- Article first published online: 13 JAN 2012
- Accepted manuscript online: 19 DEC 2011 09:40PM EST
- Received 9 November 2011, accepted 8 December 2011
There is considerable interest in the identification of natural agents capable of affording protection to skin from the adverse effects of solar ultraviolet B (UVB) radiation. Pomegranate (Punica granatum L.) fruit possesses as strong antioxidant, anti-inflammatory and antiproliferative properties. Recently, we have shown that oral feeding of pomegranate fruit extract (PFE) to mice afforded substantial protection from the adverse effects of single UVB radiation via modulation in early biomarkers of photocarcinogenesis. This study was designed to investigate the photochemopreventive effects of PFE (0.2%, wt/vol) after multiple UVB irradiations (180 mJ cm−2, on alternative day, for a total of seven treatments) to the skin of SKH-1 hairless mice. Oral feeding of PFE to SKH-1 mice inhibited UVB-induced epidermal hyperplasia, infiltration of leukocytes, protein oxidation and lipid peroxidation. Immunoblot analysis demonstrated that oral feeding of PFE to mice inhibited UVB-induced (1) nuclear translocation and phosphorylation of nuclear factor kappa B/p65, (2) phosphorylation and degradation of IκBα, (3) activation of IKKα/ΙΚΚβ and (4) phosphorylation of mitogen-activated protein kinase proteins and c-Jun. PFE consumption also inhibited UVB-induced protein expression of (1) COX-2 and iNOS, (2) PCNA and cyclin D1 and (3) matrix metalloproteinases-2,-3 and -9 in mouse skin. Taken together, these data show that PFE consumption afforded protection to mouse skin against the adverse effects of UVB radiation by modulating UVB-induced signaling pathways.