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Low-dose ultraviolet B induces sunburn reaction in Nrf2 gene-deficient mice

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Author:
No author available
Journal Title:
Chinese Journal of Dermatology
Issue:
7
DOI:
10.3760/cma.j.issn.0412-4030.2012.07.002
Key Word:
紫外线;晒伤;NF-E2相关因子2;活性氧;Keap1;Ultraviolet rays;Sunburn;NF-E2-related factor 2;Reactive oxygen species;Keap1

Abstract: [Objective] To investigate the roles of Nrf2-Keap1 system in the protection of skin from ultraviolet B (UVB)-induced damage.[Methods] The dorsal surface of ears of 8 wild-type and 8 nrf2-null mutant 8-week-old female mice was exposed to a single dose of UVB irradiation (200 mJ/cm2) by using a FL120SE UV lamp source.Then,the morphology of ears was observed with the measurement of thickness before,as well as on day 1,2,4,7,9,11 and 14 after,the irradiation.Biopsy specimens were taken from the ears 36hours after the irradiation and subjected to hematoxylin and eosin staining as well as terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.The test Results were recorded and statistically analyzed by rank sum test and t test.[Results] A significant increase was observed in the thickness of mouse ears and number of sunburn cells per high-power field (400 ×) in nrf2-null mutant mice compared with wild-type mice ((0.49 ± 0.22) cm vs.(0.25 ± 0.03) cm,P< 0.01; 17.0 ± 3.9 vs.5.0 ± 1.7,t=13.8,P< 0.01).The number of TUNEL positive cells in the nrf2-null mutant mice was about 5 times that in the wild mice.The sunburn reaction appeared more intense and persistent in nrf2-null mutant mice than in the wild mice.[Conclusion] Nrf2-Keap1 pathway may protect skin against acute UVB damage,including cell apoptosis and oxidative damage.

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