Abstract
Background and objectives: The purpose of this study was to confirm the effect of Galgeunhwanggeumhwangryeon-tang (GGRT) on the skin barrier integrity and inflammation in an atopic dermatitis-like animal model. Materials and Methods: The model was established using lipid barrier elimination (LBE) in BALB/c mice. Ceramide 3B, a control drug, and GGRT were applied to the skin of LBE mice. Gross observation and histological examination were combined with measurement of skin score, trans-epidermal water loss, and pH. The expression of filaggrin, kallikrein-related peptidase 7 (KLK7), protease-activated receptor-2 (PAR-2), thymic stromal lymphopoietin (TSLP), and interleukin 4 (IL-4) was examined. Results: The effect of GGRT on atopic dermatitis was estimated in silico using two individual gene sets of human atopic dermatitis. In animal experiments, GGRT treatment reduced atopic dermatitis-like symptoms, as confirmed via gross and histological observations, skin score, pH change, and trans-epidermal water loss. The expression level of filaggrin increased in the skin of GGRT-treated mice compared to that in the LBE group. The expression levels of KLK7, PAR2, TSLP, and IL-4 were decreased in GGRT-treated mice skin compared to those in LBE mice. Conclusions: We demonstrated that GGRT restored the skin barrier and reduced inflammatory reactions in a murine model of atopic dermatitis.
Highlights
Atopic dermatitis is a chronic inflammatory skin disease that originates from a complex interaction among various factors [1]
According to a recent systems pharmacological study that revealed the mechanism of action (MOA) of GGRT using a multi-omics approach, including transcriptomic Kyoto Encyclopedia of Genes and Genomes (KEGG)
The results showed that 12 signaling pathways, Toll-like receptor, T cell receptor, nucleotide-binding oligomerization domain (NOD)-like receptor, retinoic acid-inducible gene I (RIG-I)-like receptor, chemokine, neurotrophin, vascular endothelial cell growth factor (VEGF), sphingolipids, calcium, adipocytokine, mammalian target of rapamycin, and mitogen-activated protein kinase (MAPK), among 22 of the predicted GGRT-related pathways were commonly upregulated in the atopic dermatitis lesion (Figure 2A,C)
Summary
Atopic dermatitis is a chronic inflammatory skin disease that originates from a complex interaction among various factors [1]. Several conventional drugs including steroid, calcineurin inhibitors, and moisturizing creams, are widely, used for treating atopic dermatitis, but often they are not effective in some patients [1,4]. The purpose of this study was to confirm the effect of Galgeunhwanggeumhwangryeon-tang (GGRT) on the skin barrier integrity and inflammation in an atopic dermatitis-like animal model. GGRT treatment reduced atopic dermatitis-like symptoms, as confirmed via gross and histological observations, skin score, pH change, and trans-epidermal water loss. The expression level of filaggrin increased in the skin of GGRT-treated mice compared to that in the LBE group. The expression levels of KLK7, PAR2, TSLP, and IL-4 were decreased in GGRT-treated mice skin compared to those in LBE mice. Conclusions: We demonstrated that GGRT restored the skin barrier and reduced inflammatory reactions in a murine model of atopic dermatitis
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