Korean red ginseng water extract alleviates atopic dermatitis-like inflammatory responses by negative regulation of mitogen-activated protein kinase signaling pathway in vivo

Biomed Pharmacother. 2019 Sep:117:109066. doi: 10.1016/j.biopha.2019.109066. Epub 2019 Jun 19.

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease. Korean red ginseng is a Korean traditional medicine. In this study, we estimated the effects of Korean red ginseng water extract (RGE) in the 1-chloro-2,4-dinitrobenzene (DNCB)-induced BALB/c mouse model which develops AD-like lesions. After RGE administration (100, 200, and 400 mg/kg) to DNCB-induced mice there were improvements in the dermatitis score and skin pH, a decrease in trans-epidermal water loss, and improved skin hydration. RGE also significantly inhibited eosinophil infiltration, increased filaggrin protein levels, and decreased serum IgE levels, epidermal thickness, mast cell infiltration, and ceramidase release. Compared with that in DNCB-induced mice, RGE effectively decreased the mRNA expression levels of interleukin-6 (IL-6), thymic stromal lymphopoietin (TSLP), and tumor necrosis factor-α (TNF-α), as well as the protein level of thymus and activation-regulated chemokine (TARC). These inhibitory RGE effects are mediated by inhibiting the phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 MAPK. Furthermore, we confirmed that RGE suppresses interferon-γ (IFN-γ) and TNF-α-induced expression of macrophage-derived chemokine (MDC) and TARC genes in human keratinocyte (HaCaT) cells. Taken together, these results demonstrate that RGE may exert anti-atopic related to responses by suppression the expression of inflammatory mediators, cytokines, and chemokines via downregulation of MAPK signaling pathways, suggesting that RGE may be an effective therapeutic approach for prevention of AD-like disease.

Keywords: Atopic dermatitis; Inflammation; Korean red ginseng; Mitogen-activated protein kinase; Skin barrier.

MeSH terms

  • Animals
  • Cell Survival / drug effects
  • Chemokines / metabolism
  • Dermatitis, Atopic / drug therapy*
  • Dermatitis, Atopic / enzymology*
  • Dermatitis, Atopic / pathology
  • Dinitrochlorobenzene
  • Disease Models, Animal
  • Filaggrin Proteins
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / pathology
  • Inflammation Mediators / metabolism
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism
  • Keratinocytes / pathology
  • MAP Kinase Signaling System* / drug effects
  • Male
  • Mice, Inbred BALB C
  • Panax / chemistry*
  • Phosphorylation / drug effects
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use*
  • Skin / drug effects
  • Skin / pathology
  • Water / chemistry*
  • Water Loss, Insensible / drug effects

Substances

  • Chemokines
  • Dinitrochlorobenzene
  • FLG protein, human
  • Filaggrin Proteins
  • Inflammation Mediators
  • Plant Extracts
  • Water