Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder that can be associated with psychiatric disorders. Picrasma quassioides (D.Don) Benn (Gomokpi, GMP), a traditional medicinal herb, has been used to treat skin diseases, including AD. The current study examined the effects of an ethanolic extract of GMP on 2,4-dinitrochlorobenzene (DNCB)-induced AD mice. The severity of skin symptoms and behavioral changes in AD mice were evaluated. GMP alleviated the AD-like skin inflammation and hyperlocomotion activity in DNCB-treated BALB/c mice. The effects of GMP behavioral abnormalities might occur by inhibiting TNF-α production in the PFC. GMP suppressed the production of TARC (Th2 chemokine) in TI-stimulated HaCaT keratinocytes. Moreover, GMP also exerted immunosuppressive effects by reducing TNF-α production in LPS-stimulated Raw264.7 macrophages, IL-17 expression in PI-stimulated EL4 cells, and VEGF secretion in SP-stimulated HMC-1 cells. These findings suggest that GMP could be useful for treating AD by modulating inflammatory responses and comorbid behavioral changes.
Highlights
Atopic dermatitis (AD) is a common inflammatory skin disease that requires longterm treatment because of its frequent recurrence [1]
GMP treated groups compared to the DNCB group (Figure 2A,B)
The spleen index was reduced significantly in the DNCB group compared to the normal control group (NC) group, which was significantly lower in the GMP-treated groups (Figure 2C)
Summary
Atopic dermatitis (AD) is a common inflammatory skin disease that requires longterm treatment because of its frequent recurrence [1]. 1 (FcεRI) on the mast cell surface, leading to mast cell degranulation and the secretion of inflammatory mediators, such as histamine, cytokines, chemokines, and growth factors [5]. These degranulation substances cause and worsen AD symptoms, such as swelling and itching [6]. The inflammatory mediators produced by these immune cells can promote cytokine production and decrease the expression of skin barrier peptides in keratinocytes, leading to skin inflammation and barrier disruption in AD lesions [8]
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