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Dietary Feeding of Opuntia Humifusa Inhibits UVB Radiation‐Induced Carcinogenesis by Reducing Inflammation and Proliferation in Hairless Mouse Model
Author(s) -
Lee JinA,
Jung BockGie,
Kim TaeHoon,
Lee SuGil,
Park YoungSeok,
Lee BongJoo
Publication year - 2013
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/php.12113
Subject(s) - hairless , proinflammatory cytokine , carcinogenesis , inflammation , tumor necrosis factor alpha , chemistry , cancer research , proliferating cell nuclear antigen , pharmacology , microbiology and biotechnology , cell growth , biology , immunology , biochemistry , gene
Abstract It has been validated that ultraviolet B (UVB) irradiation induced both squamous and basal cell carcinomas, as a tumor initiator and promoter. Opuntia humifusa is a member of the Cactaceae family which has been demonstrated in our previous study to have a chemopreventive effect in 7, 12‐dimethylbenz[a]anthracene and 12‐O‐tetradecanoylphorbol‐13‐acetate induced skin carcinogenesis models. Therefore, this study was designed to determine the protective effects of O.humifusa against photocarcinogenesis. O. humifusa was administrated to mice as a dietary feeding, following exposure to UVB radiation (180 mJ/cm 2 ) twice a week of 30 weeks for skin tumor development in hairless mice. Dietary O.humifusa inhibited UVB‐induced epidermal hyperplasia, infiltration of leukocytes, level of myeloperoxidase and the levels of proinflammatory cytokines, tumor necrosis factor‐ α (TNF‐α), interleukin‐1β (IL‐1β) and interleukin‐6 (IL‐6), in UVB exposed skin. Also, O.humifusa significantly inhibited both protein and mRNA expression level of cyclooxygenase‐2 (COX‐2), nitric oxide synthase ( iNOS ), proliferating cell nuclear antigen (PCNA) and cyclin D1 compared to the non‐ O.humifusa treated group. Collectively, these results suggest that O.humifusa could inhibit photocarcinogenesis in mouse skin and that protective effect is associated with the inhibition of not only UVB‐induced inflammatory responses involving COX‐2, iNOS and proinflammatory cytokines, but also the down‐regulation of UVB‐induced cellular proliferation.