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Birmingham, AL, United States

Ahmad I.,Skin Diseases Research Center | Jimenez H.,Skin Diseases Research Center | Yaacob N.S.,Universiti Sains Malaysia | Yusuf N.,Skin Diseases Research Center | And 2 more authors.
Photochemistry and Photobiology | Year: 2012

Malaysian tualang honey possesses strong antioxidant and anti-inflammatory properties. Here, we evaluated the effect of tualang honey on early biomarkers of photocarcinogenesis employing PAM212 mouse keratinocyte cell line. Keratinocytes were treated with tualang honey (1.0%, v/v) before a single UVB (150 mJ cm-2) irradiation. We found that the treatment of tualang honey inhibited UVB-induced DNA damage, and enhanced repair of UVB-mediated formation of cyclobutane pyrimidine dimers and 8-oxo-7,8-dihydro-2'- deoxyguanosine. Treatment of tualang honey inhibited UVB-induced nuclear translocation of NF-κB and degradation of IκBα in murine keratinocyte cell line. The treatment of tualang honey also inhibited UVB-induced inflammatory cytokines and inducible nitric oxide synthase protein expression. Furthermore, the treatment of tualang honey inhibited UVB-induced COX-2 expression and PGE2 production. Taken together, we provide evidence that the treatment of tualang honey to keratinocytes affords substantial protection from the adverse effects of UVB radiation via modulation in early biomarkers of photocarcinogenesis and provide suggestion for its photochemopreventive potential. © 2012 Wiley Periodicals, Inc. Source


Nasti T.H.,Skin Diseases Research Center | Iqbal O.,Skin Diseases Research Center | Tamimi I.A.,Skin Diseases Research Center | Geise J.T.,Skin Diseases Research Center | And 6 more authors.
Photochemistry and Photobiology | Year: 2011

Ultraviolet (UV) radiation, in particular the midwavelength range (UVB; 290-320 nm), is one of the most significant risk factors for the development of nonmelanoma skin cancer. UVB radiation-induced immunosuppression, which occurs in both humans and laboratory animals, contributes to their pathogenesis. However, there are conflicting reports on the relative role of CD4+ and CD8+ T cells in UVB induced skin cancer. The purpose of this study was to delineate the contribution of these two cell subpopulations to UVB induced immunosuppression and tumor development using C3H/HeN (WT), CD4 knockout (CD4-/-) and CD8 knockout (CD8-/-) mice. We observed that UVB induced skin carcinogenesis was retarded in terms of number of tumors per group, tumor volume and percentage of mice with tumors, in mice deficient in CD4+ T cells compared with wild-type mice, whereas significantly greater (P < 0.05) numbers of tumors occurred in CD8-/- mice. These results indicate that, CD4+ T cells promote tumor development while CD8+ T cells have the opposite effect. Further, we found that CD4+ T cells from tumor-bearing mice produced interleukin (IL)-4, IL-10, and IL-17 whereas CD8+ T cells produced interferon-γ. Manipulation of T-cell subpopulations that are induced by UVB radiation could be a means of preventing skin cancers caused by this agent. © 2010 The American Society of Photobiology. Source

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