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Sulforaphane suppresses TARC/CCL17 and MDC/CCL22 expression through heme oxygenase-1 and NF-κB in human keratinocytes

Seung-Il Jeong1, Byung-Min Choi, Seon Il Jang

  • 1Jeonju Biomaterials Institute, Korea.

Archives of Pharmacal Research
|December 1, 2010
PubMed

Insights

Sulforaphane (SFN) from broccoli suppresses inflammatory chemokines in skin cells by inhibiting NF-κB and activating heme oxygenase-1 (HO-1). This finding offers potential for managing atopic dermatitis through SFN

Area of Science:

  • Dermatology
  • Immunology
  • Molecular Biology

Background:

  • Atopic dermatitis is a chronic inflammatory skin condition.
  • Sulforaphane (SFN), a broccoli-derived compound, exhibits anti-inflammatory and antioxidant properties.
  • The role of SFN in regulating Th2 chemokines via heme oxygenase-1 (HO-1) and NF-κB in keratinocytes remains unstudied.

Purpose of the Study:

  • To investigate whether SFN regulates Th2-related chemokine production in human HaCaT keratinocytes.
  • To elucidate the underlying molecular mechanisms involving HO-1 and NF-κB signaling pathways.

Main Methods:

  • Reverse transcription polymerase chain reaction (RT-PCR) for chemokine expression.
  • Western blot analysis for signaling pathway activation (NF-κB, STAT1).
  • Enzyme-linked immunosorbent assay (ELISA) for chemokine production quantification.
  • RNA interference (siRNA) to assess the role of HO-1.

Main Results:

  • SFN pretreatment suppressed interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α)-induced thymus- and activation-regulated chemokine (TARC/CCL17) and macrophage-derived chemokine (MDC/CCL22) production.
  • SFN inhibited IFN-γ and TNF-α-induced NF-κB and STAT1 activation.
  • SFN-mediated suppression of TARC/CCL17 and MDC/CCL22 was dependent on HO-1 induction, as confirmed by HO-1 siRNA experiments.
  • Carbon monoxide, an end product of HO-1, mimicked SFN's suppressive effect.

Conclusions:

  • SFN inhibits the production of Th2 chemokines (TARC/CCL17 and MDC/CCL22) in human keratinocytes.
  • This inhibition is mediated by the suppression of NF-κB activation and the induction of HO-1.
  • SFN's mechanism involves HO-1-derived carbon monoxide, suggesting a potential therapeutic strategy for inflammatory skin diseases like atopic dermatitis.

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