Current address: Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL, USA.
Oral Feeding of Pomegranate Fruit Extract Inhibits Early Biomarkers of UVB Radiation-induced Carcinogenesis in SKH-1 Hairless Mouse Epidermis
Article first published online: 14 OCT 2010
© 2010 The Authors. Journal Compilation. The American Society of Photobiology
Photochemistry and Photobiology
Volume 86, Issue 6, pages 1318–1326, November/December 2010
How to Cite
Afaq, F., Khan, N., Syed, D. N. and Mukhtar, H. (2010), Oral Feeding of Pomegranate Fruit Extract Inhibits Early Biomarkers of UVB Radiation-induced Carcinogenesis in SKH-1 Hairless Mouse Epidermis. Photochemistry and Photobiology, 86: 1318–1326. doi: 10.1111/j.1751-1097.2010.00815.x
- Issue published online: 19 NOV 2010
- Article first published online: 14 OCT 2010
- Accepted manuscript online: 23 SEP 2010 11:30AM EST
- Received 9 August 2010, accepted 6 September 2010
Pomegranate from the plant Punica granatum L. possesses strong antioxidant and anti-inflammatory properties. Recently, we have demonstrated that treatment of normal human epidermal keratinocytes with pomegranate fruit extract (PFE) inhibited UVB-mediated activation of nuclear factor kappa B (NF-κB) and mitogen activated protein kinases pathways. Here, we evaluated the effect of PFE on early biomarkers of photocarcinogenesis employing SKH-1 hairless mice. PFE was provided in drinking water (0.2%, wt/vol) to SKH-1 hairless mice for 14 days before a single UVB (180 mJ cm−2) irradiation. We found that oral feeding of PFE inhibited UVB-induced: (1) skin edema; (2) hyperplasia; (3) infiltration of leukocytes; (4) lipid peroxidation; (5) hydrogen peroxide generation; (6) ornithine decarboxylase (ODC) activity; and (7) ODC, cyclooxygenase-2 and proliferating cell nuclear antigen protein expression. Oral feeding of PFE enhanced repair of UVB-mediated formation of cyclobutane pyrimidine dimers (CPDs) and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG). Importantly, PFE treatment further enhanced UVB-mediated increase in tumor suppressor p53 and cyclin kinase inhibitor p21. Furthermore, oral feeding of PFE inhibited UVB-mediated: (1) nuclear translocation of NF-κB; (2) activation of IKKα; and (3) phosphorylation and degradation of IκBα. Taken together, we provide evidence that oral feeding of PFE to mice affords substantial protection from the adverse effects of UVB radiation via modulation in early biomarkers of photocarcinogenesis and provide suggestion for its photochemopreventive potential.