Cultivated ginseng inhibits 2,4-dinitrochlorobenzene-induced atopic dermatitis-like skin lesions in NC/Nga mice and TNF-α/IFN-γ-induced TARC activation in HaCaT cells

Food Chem Toxicol. 2013 Jun:56:195-203. doi: 10.1016/j.fct.2013.02.037. Epub 2013 Feb 27.

Abstract

Ginseng contains many bioactive constituents, including various ginsenosides that are believed to have anti-allergic, anti-oxidant, and immunostimulatory activities; however, its effects on atopic dermatitis (AD) remain unclear. In the current study, we hypothesized that cultivated ginseng (CG) would inhibit 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin lesions in NC/Nga mice by regulating the T helper (Th)1/Th2 balance. Also, CG inhibits TNF-α/IFN-γ-induced thymus- and activation-regulated chemokine (TARC) expression through nuclear factor-kappa B (NF-κB)-dependent signaling in HaCaT cells. CG ameliorated DNCB-induced dermatitis severity, serum levels of IgE and TARC, and mRNA expression of TARC, TNF-α, IFN-γ, IL-4, IL-5, and IL-13 in mice. Histopathological examination showed reduced thickness of the epidermis/dermis and dermal infiltration of inflammatory cells in the ears. Furthermore, CG suppressed the TNF-α/IFN-γ-induced mRNA expression of TARC in HaCaT cells. CG inhibited TNF-α/IFN-γ-induced NF-κB activation. These results suggest that CG inhibited the development of the AD-like skin symptoms by modulating Th1 and Th2 responses in the skin lesions in mice and TARC expression by suppressing TNF-α/IFN-γ-induced NF-κB activation in keratinocytes, and so may be a useful tool in the therapy of AD-like skin symptoms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line
  • Chemokine CCL17 / blood
  • Chemokine CCL17 / genetics
  • Chemokine CCL17 / metabolism*
  • Dermatitis, Atopic / drug therapy*
  • Dermatitis, Atopic / etiology
  • Dermatitis, Atopic / pathology
  • Dinitrochlorobenzene / adverse effects*
  • Humans
  • Immunoglobulin E / blood
  • Interferon-gamma / pharmacology*
  • Interleukin-13 / genetics
  • Interleukin-13 / metabolism
  • Interleukin-4 / genetics
  • Interleukin-4 / metabolism
  • Interleukin-5 / genetics
  • Interleukin-5 / metabolism
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism
  • Keratinocytes / pathology
  • Male
  • Mice
  • NF-kappa B / genetics
  • NF-kappa B / metabolism
  • Panax / chemistry*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Signal Transduction
  • Skin / drug effects
  • Skin / pathology
  • Th1-Th2 Balance / drug effects
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • CCL17 protein, human
  • Ccl17 protein, mouse
  • Chemokine CCL17
  • Dinitrochlorobenzene
  • Interleukin-13
  • Interleukin-5
  • NF-kappa B
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Interleukin-4
  • Immunoglobulin E
  • Interferon-gamma