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1.
J Ethnopharmacol ; 206: 327-336, 2017 Jul 12.
Article in English | MEDLINE | ID: mdl-28583294

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Hataedock treatment is traditionally used for the purpose of preventing the future skin disease by feeding herbal extracts to the newborn in traditional Chinese and Korean medicine. AIM OF THE STUDY: This study investigated the preventive therapeutic effects of Hataedock (HTD) treatment for atopic dermatitis (AD) through skin barrier protection in Dermatophagoides farinae-induced NC/Nga mice. MATERIALS AND METHODS: To the HTD treatment group, the extract of Coptis japonica Makino and Glycyrrhiza uralensis Fischer, which analyzed with High Performance Liquid Chromatography (HPLC)-fingerprint for quality consistency, was administered orally to the 3-week-old mice before inducing AD. After that, Dermatophagoides farinae was applied except the control group to induce AD-like skin lesions. We confirmed the effects of HTD on morphological changes, protection of skin barrier, regulation of Th2 differentiation, inflammation regulation and induction of apoptosis through histochemistry, immunohistochemistry, and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. RESULTS: HTD effectively reduced edema, angiogenesis and skin lesion. HTD also increased the levels of liver X receptor (LXR) and filaggrin but decreased the level of protein kinase C (PKC) (p<0.01). The levels of interleukin-4 (IL-4), IL-13, signal transducer and activator of transcription-6 (STAT-6) and Cluster of differentiation 40 (CD40) were significantly reduced in the HTD treated group (p<0.01). HTD also suppressed the mast cell degranulation and the level of the high-affinity IgE receptor (FcɛRI), substance P, Matrix metalloproteinases-9 (MMP-9) and 5-hydroxytryptamine (5-HT) (p<0.01). The levels of inflammatory factors such as nuclear factor-kappaB (NF-κB) p65, phosphorylated IκB (p-IκB) and inducible nitric oxide synthase (iNOS) were also decreased (p<0.01). Apoptosis of inflammatory cells was also found to increase (p<0.01). CONCLUSION: Our results indicate that HTD effectively regulate the Th2 differentiation, mast cell activation and various inflammatory responses on AD-induced mice through protection of skin barrier. Therefore, HTD may have potential applications for alternative and preventive treatment in the management of AD.


Subject(s)
Dermatitis, Atopic/prevention & control , Dermatophagoides farinae/immunology , Herbal Medicine , Medicine, East Asian Traditional , Animals , Cell Differentiation , Dermatitis, Atopic/pathology , Dermatitis, Atopic/therapy , Down-Regulation , Male , Mice , Skin Absorption , Th2 Cells/pathology
2.
Article in English | MEDLINE | ID: mdl-27313639

ABSTRACT

This study investigated the preventive therapeutic effects of Hataedock (HTD) treatment on inflammatory regulation and skin protection in AD-induced NC/Nga mice under high-fat diet conditions. Before inducing AD, the extract of Coptidis Rhizoma and Glycyrrhiza uralensis was administered orally to the 3-week-old mice. After that, AD-like skin lesions were induced by applying DNFB. All groups except the control group were fed a high-fat diet freely. We identified the effects of HTD on morphological changes, cytokine release and the induction of apoptosis through histochemistry, immunohistochemistry, and TUNEL assay. HTD downregulated the levels of IL-4 and PKC but increased the levels of LXR. HTD also suppressed the mast cell degranulation and release of MMP-9, Substance P. The levels of TNF-α, p-IκB, iNOS, and COX-2 were also decreased. The upregulation of inflammatory cell's apoptosis is confirmed by our results as increase of apoptotic body and cleaved caspase-3 and decrease of Bcl-2. HTD also reduced edema, angiogenesis, and skin lesion inflammation. Our results indicate HTD suppresses various inflammatory response on AD-induced mice with obesity through the regulation of Th2 differentiation and the protection of lipid barrier. Therefore, HTD could be used as an alternative and preventive therapeutic approach in the management of AD.

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