Inhibitory effect of galangin on atopic dermatitis-like skin lesions

•Galangin reduced both acute and chronic AD symptoms.•Galangin inhibited activation of human keratinocytes.•Galangin might be a candidate for the treatment of AD. Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported th...

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Veröffentlicht in:Food and chemical toxicology 2014-06, Vol.68, p.135-141
Hauptverfasser: Choi, Jin Kyeong, Kim, Sang-Hyun
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description •Galangin reduced both acute and chronic AD symptoms.•Galangin inhibited activation of human keratinocytes.•Galangin might be a candidate for the treatment of AD. Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported the inhibitory effect of galangin on the mast cell-mediated allergic inflammation. For incremental research, we investigated the effects of galangin on atopic dermatitis (AD)-like skin lesions and underlying mechanisms of action. We established an atopic dermatitis model in BALB/c mice by repeated local exposure of house dust mite (Dermatophagoides farinae) extract (DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. Topical application of galangin reduced AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. Galangin inhibited mast cell infiltration into the ear and serum histamine level. Galangin suppressed DFE/DNCB-induced expression of interleukin (IL)-4, IL-5, IL-13, IL-31, IL-32, and interferon (IFN)-γ in the ear tissue. To define the underlying mechanisms of action, tumor necrosis factor-α/IFN-γ-activated human keratinocytes (HaCaT) model was used. Galangin significantly inhibited the expression of cytokines and chemokine by the down-regulation of nuclear factor-κB and mitogen-activated protein kinases in HaCaT cells. Taken together, the results demonstrate that galangin inhibited AD-like symptoms, suggesting that galangin might be a candidate for the treatment of AD.
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Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported the inhibitory effect of galangin on the mast cell-mediated allergic inflammation. For incremental research, we investigated the effects of galangin on atopic dermatitis (AD)-like skin lesions and underlying mechanisms of action. We established an atopic dermatitis model in BALB/c mice by repeated local exposure of house dust mite (Dermatophagoides farinae) extract (DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. Topical application of galangin reduced AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. Galangin inhibited mast cell infiltration into the ear and serum histamine level. Galangin suppressed DFE/DNCB-induced expression of interleukin (IL)-4, IL-5, IL-13, IL-31, IL-32, and interferon (IFN)-γ in the ear tissue. To define the underlying mechanisms of action, tumor necrosis factor-α/IFN-γ-activated human keratinocytes (HaCaT) model was used. Galangin significantly inhibited the expression of cytokines and chemokine by the down-regulation of nuclear factor-κB and mitogen-activated protein kinases in HaCaT cells. 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Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported the inhibitory effect of galangin on the mast cell-mediated allergic inflammation. For incremental research, we investigated the effects of galangin on atopic dermatitis (AD)-like skin lesions and underlying mechanisms of action. We established an atopic dermatitis model in BALB/c mice by repeated local exposure of house dust mite (Dermatophagoides farinae) extract (DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. Topical application of galangin reduced AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. Galangin inhibited mast cell infiltration into the ear and serum histamine level. Galangin suppressed DFE/DNCB-induced expression of interleukin (IL)-4, IL-5, IL-13, IL-31, IL-32, and interferon (IFN)-γ in the ear tissue. To define the underlying mechanisms of action, tumor necrosis factor-α/IFN-γ-activated human keratinocytes (HaCaT) model was used. Galangin significantly inhibited the expression of cytokines and chemokine by the down-regulation of nuclear factor-κB and mitogen-activated protein kinases in HaCaT cells. Taken together, the results demonstrate that galangin inhibited AD-like symptoms, suggesting that galangin might be a candidate for the treatment of AD.</description><subject>Acute Disease</subject><subject>Allergic diseases</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antigens, Dermatophagoides - pharmacology</subject><subject>Antioxidants - pharmacology</subject><subject>Atopic dermatitis</subject><subject>Biological and medical sciences</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Chronic Disease</subject><subject>Dermatitis, Atopic - drug therapy</subject><subject>Dermatophagoides farinae</subject><subject>Dermatophagoides pteronyssinus</subject><subject>Dinitrochlorobenzene - pharmacology</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Flavonoids - pharmacology</subject><subject>Food toxicology</subject><subject>Galangin</subject><subject>Histamine - blood</subject><subject>Humans</subject><subject>Immunoglobulins - blood</subject><subject>Immunopathology</subject><subject>Interferon-gamma - genetics</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukins - genetics</subject><subject>Interleukins - metabolism</subject><subject>Keratinocyte</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Mast cells</subject><subject>Mast Cells - drug effects</subject><subject>Mast Cells - metabolism</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mitogen-Activated Protein Kinases - genetics</subject><subject>Mitogen-Activated Protein Kinases - metabolism</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>Skin allergic diseases. Stinging insect allergies</subject><subject>Toxicology</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0278-6915</issn><issn>1873-6351</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAURa2qqAy0P6CbKptKbBKe7dhx1FXFt4TEhq4t8_JMPWTiwc4g8e_xaIZ2x-ot3rlXV4ex7xwaDlyfLhuPcyOAtw3IBgT_xBbcdLLWUvHPbAGiM7XuuTpkRzkvAaDjnf7CDkWrO9UKsWDnN9Pf8BDmmF4r8p5wrqKvHt3opscwVXGq3BzXAauB0srNYQ65HsMTVfmpvEfKIU75Kzvwbsz0bX-P2Z_Li_uz6_r27urm7Pdtja0Rc61BeoFgwKPuzcB97zsH2gjT42CMHiToAR045NSDJo1aQtsp0ypSqFEes5Nd7zrF5w3l2a5CRhrLWIqbbLkWQgNXnSoo36GYYs6JvF2nsHLp1XKwW3l2aYs8u5VnQdoir2R-7Os3Dysa_iXebRXg5x5wGd3ok5sw5P-cUSDBbIt-7TgqMl4CJZsx0IQ0hFQM2yGGD2a8AUdei2s</recordid><startdate>20140601</startdate><enddate>20140601</enddate><creator>Choi, Jin Kyeong</creator><creator>Kim, Sang-Hyun</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20140601</creationdate><title>Inhibitory effect of galangin on atopic dermatitis-like skin lesions</title><author>Choi, Jin Kyeong ; Kim, Sang-Hyun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-603f2c080fc698d1f9f7a068289cd886d306dca0ac1e906e6c630475845e5c6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Acute Disease</topic><topic>Allergic diseases</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antigens, Dermatophagoides - pharmacology</topic><topic>Antioxidants - pharmacology</topic><topic>Atopic dermatitis</topic><topic>Biological and medical sciences</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Chronic Disease</topic><topic>Dermatitis, Atopic - drug therapy</topic><topic>Dermatophagoides farinae</topic><topic>Dermatophagoides pteronyssinus</topic><topic>Dinitrochlorobenzene - pharmacology</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Flavonoids - pharmacology</topic><topic>Food toxicology</topic><topic>Galangin</topic><topic>Histamine - blood</topic><topic>Humans</topic><topic>Immunoglobulins - blood</topic><topic>Immunopathology</topic><topic>Interferon-gamma - genetics</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukins - genetics</topic><topic>Interleukins - metabolism</topic><topic>Keratinocyte</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Mast cells</topic><topic>Mast Cells - drug effects</topic><topic>Mast Cells - metabolism</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mitogen-Activated Protein Kinases - genetics</topic><topic>Mitogen-Activated Protein Kinases - metabolism</topic><topic>NF-kappa B - genetics</topic><topic>NF-kappa B - metabolism</topic><topic>Skin allergic diseases. Stinging insect allergies</topic><topic>Toxicology</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Jin Kyeong</creatorcontrib><creatorcontrib>Kim, Sang-Hyun</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Food and chemical toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Jin Kyeong</au><au>Kim, Sang-Hyun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibitory effect of galangin on atopic dermatitis-like skin lesions</atitle><jtitle>Food and chemical toxicology</jtitle><addtitle>Food Chem Toxicol</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>68</volume><spage>135</spage><epage>141</epage><pages>135-141</pages><issn>0278-6915</issn><eissn>1873-6351</eissn><coden>FCTOD7</coden><abstract>•Galangin reduced both acute and chronic AD symptoms.•Galangin inhibited activation of human keratinocytes.•Galangin might be a candidate for the treatment of AD. Galangin is a member of the flavonol class of flavonoids having anti-inflammatory and anti-oxidative potential. Previously we reported the inhibitory effect of galangin on the mast cell-mediated allergic inflammation. For incremental research, we investigated the effects of galangin on atopic dermatitis (AD)-like skin lesions and underlying mechanisms of action. We established an atopic dermatitis model in BALB/c mice by repeated local exposure of house dust mite (Dermatophagoides farinae) extract (DFE) and 2,4-dinitrochlorobenzene (DNCB) to the ears. Repeated alternative treatment of DFE/DNCB caused AD-like skin lesions. Topical application of galangin reduced AD symptoms based on ear thickness and histopathological analysis, in addition to serum IgE and IgG2a levels. Galangin inhibited mast cell infiltration into the ear and serum histamine level. Galangin suppressed DFE/DNCB-induced expression of interleukin (IL)-4, IL-5, IL-13, IL-31, IL-32, and interferon (IFN)-γ in the ear tissue. To define the underlying mechanisms of action, tumor necrosis factor-α/IFN-γ-activated human keratinocytes (HaCaT) model was used. Galangin significantly inhibited the expression of cytokines and chemokine by the down-regulation of nuclear factor-κB and mitogen-activated protein kinases in HaCaT cells. Taken together, the results demonstrate that galangin inhibited AD-like symptoms, suggesting that galangin might be a candidate for the treatment of AD.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>24675422</pmid><doi>10.1016/j.fct.2014.03.021</doi><tpages>7</tpages></addata></record>
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subjects Acute Disease
Allergic diseases
Animals
Anti-Inflammatory Agents - pharmacology
Antigens, Dermatophagoides - pharmacology
Antioxidants - pharmacology
Atopic dermatitis
Biological and medical sciences
Cell Survival - drug effects
Cells, Cultured
Chronic Disease
Dermatitis, Atopic - drug therapy
Dermatophagoides farinae
Dermatophagoides pteronyssinus
Dinitrochlorobenzene - pharmacology
Down-Regulation
Female
Flavonoids - pharmacology
Food toxicology
Galangin
Histamine - blood
Humans
Immunoglobulins - blood
Immunopathology
Interferon-gamma - genetics
Interferon-gamma - metabolism
Interleukins - genetics
Interleukins - metabolism
Keratinocyte
Keratinocytes - drug effects
Keratinocytes - metabolism
Mast cells
Mast Cells - drug effects
Mast Cells - metabolism
Medical sciences
Mice
Mice, Inbred BALB C
Mitogen-Activated Protein Kinases - genetics
Mitogen-Activated Protein Kinases - metabolism
NF-kappa B - genetics
NF-kappa B - metabolism
Skin allergic diseases. Stinging insect allergies
Toxicology
Tumor Necrosis Factor-alpha - genetics
Tumor Necrosis Factor-alpha - metabolism
title Inhibitory effect of galangin on atopic dermatitis-like skin lesions
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