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Impact of Nrf2 on UVB-induced skin inflammation/photoprotection and photoprotective effect of sulforaphane

✍ Scribed by Constance L. Saw; Mou-Tuan Huang; Yue Liu; Tin Oo Khor; Allan H. Conney; Ah-Ng Kong


Book ID
102500439
Publisher
John Wiley and Sons
Year
2010
Tongue
English
Weight
464 KB
Volume
50
Category
Article
ISSN
0899-1987

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✦ Synopsis


Abstract

Ultraviolet (UV) of sunlight is a complete carcinogen that can burn skin, enhance inflammation, and drive skin carcinogenesis. Previously, we have shown that sulforaphane (SFN) inhibited chemically induced skin carcinogenesis via nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2) and others have shown that broccoli sprout extracts containing high SFN protected against UV‐induced skin carcinogenesis in SKH‐1 hairless mice. A recent study showed that there was no difference between Nrf2 knockout (Nrf2 KO) and Nrf2 wild‐type (WT) BALB/C mice after exposing to high dose of UVB. Since Nrf2 plays critical roles in the anti‐oxidative stress/anti‐inflammatory responses, it is relevant to assess the role of Nrf2 for photoprotection against UV. In this context, the role of Nrf2 in UVB‐induced skin inflammation in Nrf2 WT and Nrf2 KO C57BL/6 mice was studied. A single dose of UVB (300 mJ/cm^2^) resulted in skin inflammation in both WT and Nrf2 KO (−/−) mice (KO mice) at 8 h and 8 d following UVB irradiation. In the WT mice inflammation returned to the basal level to a greater extent when compared to the KO mice. SFN treatment of Nrf2 WT but not Nrf2 KO mice restored the number of sunburn cells back to their basal level by 8 d after UVB irradiation. Additionally, UVB‐induced short‐term inflammatory biomarkers (interleukin‐1β and interleukin‐6) were increased in the KO mice and UVB‐induced apoptotic cells in the KO mice were significantly higher as compared to that in the WT. Taken together, our results show that functional Nrf2 confers a protective effect against UVB‐induced inflammation, sunburn reaction, and SFN‐mediated photoprotective effects in the skin. © 2010 Wiley‐Liss, Inc.


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