Anti-Atopic Dermatitis Effect of <i>Seaweed Fulvescens</i> Extract via Inhibiting the STAT1 Pathway

Gil, Tae‐Young; Kang, Yun‐Mi; Eom, Ye-Jin; Hong, Chul-Hee; An, Hyo‐Jin

doi:10.1155/2019/3760934

Cited by 13 publications

(16 citation statements)

References 45 publications

(49 reference statements)

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“…Manual searching of the list of up-regulated proteins identified several of relevance to atopic eczema, including: STAT1, an intracellular signalling molecule that shows increased expression in atopic eczema, and as part of the JAK-STAT pathway is targeted by several traditional herbal remedies 44 as well as novel small molecule therapies 45 ; carbonic anhydrase 2, which is increased in skin in a variety of forms of eczema 46 ; and FK binding protein, which binds to tacrolimus, an established topical treatment for atopic eczema.…”

Section: Resultsmentioning

confidence: 99%

Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model

Elias¹,

Wright²,

Nicholson³

et al. 2019

Wellcome Open Res

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Background: Atopic eczema is an itchy inflammatory disorder characterised by skin barrier dysfunction. Loss-of-function mutations in the gene encoding filaggrin ( FLG) are a major risk factor, but the mechanisms by which filaggrin haploinsufficiency leads to atopic inflammation remain incompletely understood. Skin as an organ that can be modelled using primary cells in vitro provides the opportunity for selected genetic effects to be investigated in detail. Methods: Primary human keratinocytes and donor-matched primary fibroblasts from healthy individuals were used to create skin organoid models with and without siRNA-mediated knockdown of FLG. Biological replicate sets of organoids were assessed using histological, functional and biochemical measurements. Results: FLG knockdown leads to subtle changes in histology and ultrastructure including a reduction in thickness of the stratum corneum and smaller, less numerous keratohyalin granules. Immature organoids showed some limited evidence of barrier impairment with FLG knockdown, but the mature organoids showed no difference in transepidermal water loss, water content or dye penetration. There was no difference in epidermal ceramide content. Mass spectrometry proteomic analysis detected >8000 proteins per sample. Gene ontology and pathway analyses identified an increase in transcriptional and translational activity but a reduction in proteins contributing to terminal differentiation, including caspase 14, dermokine, AKT1 and TGF-beta-1. Aspects of innate and adaptive immunity were represented in both the up-regulated and down-regulated protein groups, as was the term ‘axon guidance’. Conclusions: This work provides further evidence for keratinocyte-specific mechanisms contributing to immune and neurological, as well as structural, aspects of skin barrier dysfunction. Individuals with filaggrin deficiency may derive benefit from future therapies targeting keratinocyte-immune crosstalk and neurogenic pruritus.

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Section: Resultsmentioning

confidence: 99%

Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model

Elias¹,

Wright²,

Nicholson³

et al. 2019

Wellcome Open Res

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“…The STAT1 signaling pathway is one of the main inflammatory signaling pathways activated by several inflammatory cytokines, such as interleukins and interferons [ 47 , 48 ]. Upon receptor stimulation by inflammatory cytokines, a typical cell surface receptor, receptor-associated JAK2, is phosphorylated.…”

Section: Discussionmentioning

confidence: 99%

Impressic Acid Ameliorates Atopic Dermatitis-Like Skin Lesions by Inhibiting ERK1/2-Mediated Phosphorylation of NF-κB and STAT1

Choi

Lee

Jin

et al. 2021

IJMS

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Impressic acid (IPA), a lupane-type triterpenoid from Acanthopanax koreanum, has many pharmacological activities, including the attenuation of vascular endothelium dysfunction, cartilage destruction, and inflammatory diseases, but its influence on atopic dermatitis (AD)-like skin lesions is unknown. Therefore, we investigated the suppressive effect of IPA on 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin symptoms in mice and the underlying mechanisms in cells. IPA attenuated the DNCB-induced increase in the serum concentrations of IgE and thymic stromal lymphopoietin (TSLP), and in the mRNA levels of thymus and activation regulated chemokine(TARC), macrophage derived chemokine (MDC), interleukin-4 (IL-4), interleukin-5 (IL-5), interleukin-13 (IL-13), tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) in mice. Histopathological analysis showed that IPA reduced the epidermal/dermal thickness and inflammatory and mast cell infiltration of ear tissue. In addition, IPA attenuated the phosphorylation of NF-κB and IκBα, and the degradation of IκBα in ear lesions. Furthermore, IPA treatment suppressed TNF-α/IFN-γ-induced TARC expression by inhibiting the NF-κB activation in cells. Phosphorylation of extracellular signalregulated protein kinase (ERK1/2) and the signal transducer and activator of transcription 1 (STAT1), the upstream signaling proteins, was reduced by IPA treatment in HaCaT cells. In conclusion, IPA ameliorated AD-like skin symptoms by regulating cytokine and chemokine production and so has therapeutic potential for AD-like skin lesions.

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“…In this study, AA treatment suppressed collagen deposition and IL-13 mRNA expression levels ( Figure 5 F,G and Figure 6 H). Furthermore, chronic AD has been characterized to upregulate Th1-related pathways and influence tissue remodeling by increasing collagen deposition and dermal thickness [ 34 ]. Similarly, we determined that the dermal and epidermal thickness in mice in the AD + AA-H group was notably diminished compared to that in the AD-only group ( Figure 5 B,C).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, AA treatment inhibited the expression levels of COX-2, CXCL9, IL-6, TNF-α, and IL-8 in this study ( Figure 7 A). Regulation of COX-2 expression led to a downregulated inflammatory response in a DNCB-induced animal model [ 34 ]. Hence, we conclude that AA can inhibit the expression of anti-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Immunomodulatory and Anti-inflammatory Effects of Asiatic Acid in a DNCB-Induced Atopic Dermatitis Animal Model

et al. 2021

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We examined the immunomodulatory and anti-inflammatory effects of asiatic acid (AA) in atopic dermatitis (AD). AA treatment (5–20 µg/mL) dose-dependently suppressed the tumor necrosis factor (TNF)-α level and interleukin (IL)-6 protein expression in interferon (IFN)-γ + TNF-α-treated HaCaT cells. The 2,4-dinitrocholrlbenzene (DNCB)-induced AD animal model was developed by administering two AA concentrations (30 and 75 mg/kg/d: AD + AA-L and AD + AA-H groups, respectively) for 18 days. Interestingly, AA treatment decreased AD skin lesions formation and affected other AD characteristics, such as increased ear thickness, lymph node and spleen size, dermal and epidermal thickness, collagen deposition, and mast cell infiltration in dorsal skin. In addition, in the DNCB-induced AD animal model, AA treatment downregulated the mRNA expression level of AD-related cytokines, such as Th1- (TNF-α and IL-1β and -12) and Th2 (IL-4, -5, -6, -13, and -31)-related cytokines as well as that of cyclooxygenase-2 and CXCL9. Moreover, in the AA treatment group, the protein level of inflammatory cytokines, including COX-2, IL-6, TNF-α, and IL-8, as well as the NF-κB and MAPK signaling pathways, were decreased. Overall, our study confirmed that AA administration inhibited AD skin lesion formation via enhancing immunomodulation and inhibiting inflammation. Thus, AA can be used as palliative medication for regulating AD symptoms.

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Anti-Atopic Dermatitis Effect of Seaweed Fulvescens Extract via Inhibiting the STAT1 Pathway

Cited by 13 publications

References 45 publications

Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model

Functional and proteomic analysis of a full thickness filaggrin-deficient skin organoid model

Impressic Acid Ameliorates Atopic Dermatitis-Like Skin Lesions by Inhibiting ERK1/2-Mediated Phosphorylation of NF-κB and STAT1

Immunomodulatory and Anti-inflammatory Effects of Asiatic Acid in a DNCB-Induced Atopic Dermatitis Animal Model

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