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      Anti-Inflammatory Effect of Chloroform Fraction of Pyrus Ussuriensis Maxim. Leaf Extract on 2, 4-Dinitrochlorobenzene-Induced Atopic Dermatitis in nc/nga Mice

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          Abstract

          Pyrus ussuriensis Maxim, a pear commonly known as “Sandolbae” in Korea, is used as a traditional herbal medicine for asthma, cough, and fever in Korea, China, and Japan. P. ussuriensis Maxim leaves (PUL) have therapeutic effects on atopic dermatitis (AD). However, there are no reports on the efficacy of specific components of PUL. In the present study, activity-guided isolation of PUL was used to determine the compounds with potent activity. Astragalin was identified as the major component of the chloroform-soluble fraction of PUL (PULC) using High-performance liquid chromatography (HPLC) analysis. Astragalin and PULC were tested in vitro and in vivo for their effects against AD. PULC and astragalin dose-dependently inhibited the production of nitric oxide (NO) in mouse macrophage (RAW 264.7) cells, and interleukin (IL)-6 and IL-1β in tumor necrosis factor (TNF-α)/interferon γ (IFNγ) induced HaCaT cells. In the AD mice model, PULC and astragalin application significantly reduced dermatitis severity, scratching behavior, and trans-epidermal water loss (TEWL) when compared to that of 2, 4-dinitrochlorobenzene-treated NC/Nga mice. Additionally, they normalized skin barrier function by decreasing immunoglobulin E (IgE) levels in the serum. Filaggrin and involucrin protein levels were normalized by PULC treatment in HaCaT cells and skin lesions. These results indicate that PULC and astragalin ameliorate AD-like symptoms by alleviating both pro-inflammatory cytokines and immune stimuli in vitro and in vivo in animal models. Therefore, PULC and astragalin might be effective therapeutic agents for the treatment of AD.

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          New insights into atopic dermatitis.

          Atopic dermatitis is a chronic inflammatory skin disease associated with cutaneous hyperreactivity to environmental triggers and is often the first step in the atopic march that results in asthma and allergic rhinitis. The clinical phenotype that characterizes atopic dermatitis is the product of interactions between susceptibility genes, the environment, defective skin barrier function, and immunologic responses. This review summarizes recent progress in our understanding of the pathophysiology of atopic dermatitis and the implications for new management strategies.
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            Adverse effects of topical glucocorticosteroids.

            Topical corticosteroids were introduced into medicine about 50 years ago. They represent a significant milestone in dermatologic therapy. Despite encouragement to report observed adverse drug reactions, the clinical practice of reporting is poor and incomplete. Likewise, adverse effects and safety of topical corticosteroids are neglected in the medical literature. The authors provide an updated review of their adverse-effect profile. Children are more prone to the development of systemic reactions to topically applied medication because of their higher ratio of total body surface area to body weight. Cutaneous adverse effects occur regularly with prolonged treatment and are dependent on the chemical nature of the drug, the vehicle, and the location of its application. The most frequent adverse effects include atrophy, striae, rosacea, perioral dermatitis, acne, and purpura. Those that occur with lower frequency include hypertrichosis, pigmentation alterations, delayed wound healing, and exacerbation of skin infections. Of particular interest is the rate of contact sensitization against corticosteroids, which is considerably higher than generally believed. Systemic reactions such as hyperglycemia, glaucoma, and adrenal insufficiency have also been reported to follow topical application. The authors provide an updated review of local and systemic adverse effects upon administration of topical corticosteroids, including the latest FDA report on the safety of such steroids in children. At the completion of this learning activity, participants should be familiar with topical corticosteroids and their proper use.
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              Immune mechanisms leading to atopic dermatitis.

              The incidence of atopic dermatitis is increasing, and this poses a major burden on health care costs. A precise understanding of the genetic and immunologic mechanisms is crucial for development of effective treatment strategies for atopic dermatitis. Various studies indicate that it has a multifactorial cause, with activation of complex immunologic and inflammatory pathways. The current review will examine recent advances that have been made in our understanding of the genetic and pathophysiologic prerequisites that form the basis of this common recalcitrant skin disorder.
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                Author and article information

                Journal
                Nutrients
                Nutrients
                nutrients
                Nutrients
                MDPI
                2072-6643
                27 January 2019
                February 2019
                : 11
                : 2
                : 276
                Affiliations
                [1 ]College of Pharmacy, Gachon University, 191, Hambakmoero, Yeonsu-gu, Incheon 21936, Korea; kcho3138@ 123456gmail.com (K.C.); mincjf07@ 123456gmail.com (M.C.K.); amnaparvin@ 123456gmail.com (A.P.)
                [2 ]Gachon Institute of Pharmaceutical Science, Gachon University, 191, Hambakmoe-ro, Yeonsu-gu, Incheon 21936, Korea
                [3 ]Department of Pharmacognosy, Faculty of Pharmaceutical Science, Government College University, Faisalabad 38000, Pakistan
                [4 ]Gachon Medical Research Institute, Gil Medical Center, Incheon 21565, Korea
                Author notes
                [* ]Correspondence: silviayumnam@ 123456gmail.com (S.Y.); sunnykim@ 123456gachon.ac.kr (S.Y.K.); Tel.: +82-32-820-4932 (S.Y.); +82-32-820-4931 (S.Y.K.)
                [†]

                The authors contributed equally to this paper.

                Author information
                https://orcid.org/0000-0001-8044-5613
                Article
                nutrients-11-00276
                10.3390/nu11020276
                6412787
                30691219
                c908b73e-31b4-48ee-b692-6097347d5967
                © 2019 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 02 January 2019
                : 23 January 2019
                Categories
                Article

                Nutrition & Dietetics
                atopic dermatitis,dncb-induced-nc/nga mice,astragalin,tnf-α/ifnγ,il-6,pulc
                Nutrition & Dietetics
                atopic dermatitis, dncb-induced-nc/nga mice, astragalin, tnf-α/ifnγ, il-6, pulc

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