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Cyanidin does not affect sulforaphane-mediated Nrf2 induction in cultured human keratinocytes

I M A Ernst1, A E Wagner, P Huebbe

  • 1Institute of Human Nutrition and Food Science, Christian-Albrechts-University Kiel, Hermann-Rodewald-Strasse 6, Kiel, Germany.

The British Journal of Nutrition
|July 13, 2011
PubMed

Insights

Cyanidin, a plant flavonoid, does not activate the Nrf2 pathway in human skin cells. Co-application with sulforaphane (SFN) did not enhance SFN-induced Nrf2 activation or gene expression.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Pharmacology

Background:

  • Isothiocyanates and flavonoids are plant compounds with gene-regulatory activities in human skin.
  • Sulforaphane (SFN), an isothiocyanate, is a known Nrf2 agonist with chemopreventive effects.
  • Interactions between plant compounds can modulate SFN-induced Nrf2 activation.

Purpose of the Study:

  • To investigate the interaction between cyanidin (a flavonoid) and SFN in human keratinocytes.
  • To determine if cyanidin affects Nrf2 activation and its downstream target genes.
  • To assess if cyanidin enhances SFN-mediated Nrf2 activation.

Main Methods:

  • Cultured human keratinocytes (HaCaT cells) were used.
  • Cells were treated with cyanidin, SFN, or a combination of both.
  • Nrf2 activation and the expression of its target genes (γGCS, NQO1, HO-1) were measured.

Main Results:

  • Cyanidin alone did not induce Nrf2 activation or the expression of its target genes in HaCaT cells.
  • SFN treatment activated Nrf2 and its target genes.
  • Co-application of SFN with cyanidin did not further enhance SFN-mediated Nrf2 activation or target gene expression.

Conclusions:

  • Cyanidin does not possess Nrf2-activating properties in human keratinocytes.
  • Cyanidin does not synergistically enhance the Nrf2-activating effects of SFN.
  • These findings suggest that cyanidin may not be a suitable co-treatment to boost SFN's chemopreventive effects via Nrf2 activation in skin.

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