Brief Communication

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

  1. Constance L. Saw1,2,
  2. Mou-Tuan Huang1,3,
  3. Yue Liu1,3,
  4. Tin Oo Khor1,2,
  5. Allan H. Conney1,3,
  6. Ah-Ng Kong1,2,*

Article first published online: 28 DEC 2010

DOI: 10.1002/mc.20725

Issue

Molecular Carcinogenesis

Molecular Carcinogenesis

Volume 50, Issue 6, pages 479–486, June 2011

Additional Information

How to Cite

Saw, C. L., Huang, M.-T., Liu, Y., Khor, T. O., Conney, A. H. and Kong, A.-N. (2011), Impact of Nrf2 on UVB-induced skin inflammation/photoprotection and photoprotective effect of sulforaphane. Mol. Carcinog., 50: 479–486. doi: 10.1002/mc.20725

Author Information

  1. 1

    Center for Cancer Prevention Research, Rutgers, The State University of New Jersey, Piscataway, New Jersey

  2. 2

    Department of Pharmaceutics, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey

  3. 3

    Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, New Jersey

*Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Room 228, 160 Frelinghuysen Road, Piscataway, NJ 08854.

Publication History

  1. Issue published online: 9 MAY 2011
  2. Article first published online: 28 DEC 2010
  3. Manuscript Accepted: 19 NOV 2010
  4. Manuscript Revised: 6 NOV 2010
  5. Manuscript Received: 4 AUG 2010

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Keywords:

  • sulforaphane;
  • nuclear factor-erythroid 2-related factor 2;
  • ultraviolet;
  • inflammation;
  • photoprotection

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/cm2) 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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