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Therapeutic Effect of Rumex japonicus Houtt. on DNCB-Induced Atopic Dermatitis-Like Skin Lesions in Balb/c Mice and Human Keratinocyte HaCaT Cells
Houtt. (RJ) is traditionally used in folk medicines to treat patients suffering from skin disease in Korea and other parts of East Asia. However, the beneficial effect of RJ extract on atopic dermatitis (AD) has not been thoroughly examined. Therefore, this study aimed to investigate the anti-inflam...
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Published in: | Nutrients 2019-03, Vol.11 (3), p.573 |
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description | Houtt. (RJ) is traditionally used in folk medicines to treat patients suffering from skin disease in Korea and other parts of East Asia. However, the beneficial effect of RJ extract on atopic dermatitis (AD) has not been thoroughly examined. Therefore, this study aimed to investigate the anti-inflammatory effects of RJ on AD in vitro and in vivo. Treatment with RJ inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) as well as the activation of nuclear factor-kappa B (NF-κB) in tumor necrosis factor-α (TNF-α) stimulated in HaCaT cells. The five-week-old Balb/c mice were used as an AD-like mouse model by treating them with 1-chloro-2, 4-dinitrobenzene (DNCB). Topical administration of RJ to DNCB-treated mice significantly reduced clinical dermatitis severity, epidermal thickness, and decreased mast cell and eosinophil infiltration into skin and ear tissue. These results suggest that RJ inhibits the development of AD-like skin lesions by regulating the skin inflammation responses in HaCaT cells and Balb/c mice. Thus, RJ may be a potential therapeutic agent for AD. |
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(RJ) is traditionally used in folk medicines to treat patients suffering from skin disease in Korea and other parts of East Asia. However, the beneficial effect of RJ extract on atopic dermatitis (AD) has not been thoroughly examined. Therefore, this study aimed to investigate the anti-inflammatory effects of RJ on AD in vitro and in vivo. Treatment with RJ inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) as well as the activation of nuclear factor-kappa B (NF-κB) in tumor necrosis factor-α (TNF-α) stimulated in HaCaT cells. The five-week-old Balb/c mice were used as an AD-like mouse model by treating them with 1-chloro-2, 4-dinitrobenzene (DNCB). Topical administration of RJ to DNCB-treated mice significantly reduced clinical dermatitis severity, epidermal thickness, and decreased mast cell and eosinophil infiltration into skin and ear tissue. These results suggest that RJ inhibits the development of AD-like skin lesions by regulating the skin inflammation responses in HaCaT cells and Balb/c mice. Thus, RJ may be a potential therapeutic agent for AD.</description><identifier>ISSN: 2072-6643</identifier><identifier>EISSN: 2072-6643</identifier><identifier>DOI: 10.3390/nu11030573</identifier><identifier>PMID: 30866501</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>AKT protein ; Atopic dermatitis ; Cytokines ; Dermatitis ; DNCB ; Eczema ; Immune response ; Immune system ; Inflammation ; Kinases ; Laboratory animals ; Lesions ; Lymph nodes ; MAP kinase ; MAPK ; NF-κB ; NF-κB protein ; Organs ; Pathogenesis ; Penicillin ; Phosphorylation ; Rumex japonicus Houtt ; Skin ; Skin diseases ; skin lesion ; Skin lesions ; Spleen ; TNF-α ; Topical application ; Translocation</subject><ispartof>Nutrients, 2019-03, Vol.11 (3), p.573</ispartof><rights>2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 by the authors. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-d2fd63ad4e08b2848b4d0cbfdb9fdcb005ecd91b6f638750cdceb015300c09af3</citedby><cites>FETCH-LOGICAL-c472t-d2fd63ad4e08b2848b4d0cbfdb9fdcb005ecd91b6f638750cdceb015300c09af3</cites><orcidid>0000-0002-5114-5096 ; 0000-0002-0844-1009</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2302282885/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2302282885?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25752,27923,27924,37011,37012,44589,53790,53792,74997</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30866501$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Hye Ryeon</creatorcontrib><creatorcontrib>Lee, Hyunkyoung</creatorcontrib><creatorcontrib>Kim, Jong-Hyun</creatorcontrib><creatorcontrib>Hong, Il-Hwa</creatorcontrib><creatorcontrib>Hwang, Du Hyeon</creatorcontrib><creatorcontrib>Rho, Il Rae</creatorcontrib><creatorcontrib>Kim, Gon Sup</creatorcontrib><creatorcontrib>Kim, Euikyung</creatorcontrib><creatorcontrib>Kang, Changkeun</creatorcontrib><title>Therapeutic Effect of Rumex japonicus Houtt. on DNCB-Induced Atopic Dermatitis-Like Skin Lesions in Balb/c Mice and Human Keratinocyte HaCaT Cells</title><title>Nutrients</title><addtitle>Nutrients</addtitle><description>Houtt. (RJ) is traditionally used in folk medicines to treat patients suffering from skin disease in Korea and other parts of East Asia. However, the beneficial effect of RJ extract on atopic dermatitis (AD) has not been thoroughly examined. Therefore, this study aimed to investigate the anti-inflammatory effects of RJ on AD in vitro and in vivo. Treatment with RJ inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) as well as the activation of nuclear factor-kappa B (NF-κB) in tumor necrosis factor-α (TNF-α) stimulated in HaCaT cells. The five-week-old Balb/c mice were used as an AD-like mouse model by treating them with 1-chloro-2, 4-dinitrobenzene (DNCB). Topical administration of RJ to DNCB-treated mice significantly reduced clinical dermatitis severity, epidermal thickness, and decreased mast cell and eosinophil infiltration into skin and ear tissue. These results suggest that RJ inhibits the development of AD-like skin lesions by regulating the skin inflammation responses in HaCaT cells and Balb/c mice. Thus, RJ may be a potential therapeutic agent for AD.</description><subject>AKT protein</subject><subject>Atopic dermatitis</subject><subject>Cytokines</subject><subject>Dermatitis</subject><subject>DNCB</subject><subject>Eczema</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lesions</subject><subject>Lymph nodes</subject><subject>MAP kinase</subject><subject>MAPK</subject><subject>NF-κB</subject><subject>NF-κB protein</subject><subject>Organs</subject><subject>Pathogenesis</subject><subject>Penicillin</subject><subject>Phosphorylation</subject><subject>Rumex japonicus Houtt</subject><subject>Skin</subject><subject>Skin diseases</subject><subject>skin lesion</subject><subject>Skin lesions</subject><subject>Spleen</subject><subject>TNF-α</subject><subject>Topical application</subject><subject>Translocation</subject><issn>2072-6643</issn><issn>2072-6643</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkstu1DAUhiMEolXphgdAltggpLQncS7OBqlNCzNiAAmGteVr62liD74g-ho8MW6nlBZvfGR__s_R778oXlZwhPEAxzZVFWBoe_yk2K-hr8uua_DTB_VecRjCBm5WD32Hnxd7GEjXtVDtF7_Xl8qzrUrRCHSutRIROY2-pln9Qhu2ddaIFNDCpRiPkLPo7PN4Wi6tTEJJdBLdNr87U35m0UQTypW5UujblbFopYJxNqBcnrKJHwv0yQiFmJVokWZm0cfcOBrrxHVUaMFGtkajmqbwonim2RTU4d1-UHx_f74eF-Xqy4fleLIqRdPXsZS1lh1mslFAeE0awhsJgmvJBy0FB2iVkEPFO91h0rcgpFAcqhYDCBiYxgfFcqcrHdvQrTcz89fUMUNvD5y_oMxnWyZFGeFYc9JwNgyNZmRQrO-5gKZtFINbrXc7rW3is8qdbPRseiT6-MaaS3rhftKu6YH0JAu8uRPw7kdSIdLZBJHtYFa5FGhdDRVucf7AjL7-D9245G22itYY6prUhLSZerujhHcheKXvh6mA3iSH_ktOhl89HP8e_ZsT_AcnOb-Q</recordid><startdate>20190307</startdate><enddate>20190307</enddate><creator>Yang, Hye Ryeon</creator><creator>Lee, Hyunkyoung</creator><creator>Kim, Jong-Hyun</creator><creator>Hong, Il-Hwa</creator><creator>Hwang, Du Hyeon</creator><creator>Rho, Il Rae</creator><creator>Kim, Gon Sup</creator><creator>Kim, Euikyung</creator><creator>Kang, Changkeun</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-5114-5096</orcidid><orcidid>https://orcid.org/0000-0002-0844-1009</orcidid></search><sort><creationdate>20190307</creationdate><title>Therapeutic Effect of Rumex japonicus Houtt. on DNCB-Induced Atopic Dermatitis-Like Skin Lesions in Balb/c Mice and Human Keratinocyte HaCaT Cells</title><author>Yang, Hye Ryeon ; Lee, Hyunkyoung ; Kim, Jong-Hyun ; Hong, Il-Hwa ; Hwang, Du Hyeon ; Rho, Il Rae ; Kim, Gon Sup ; Kim, Euikyung ; Kang, Changkeun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-d2fd63ad4e08b2848b4d0cbfdb9fdcb005ecd91b6f638750cdceb015300c09af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>AKT protein</topic><topic>Atopic dermatitis</topic><topic>Cytokines</topic><topic>Dermatitis</topic><topic>DNCB</topic><topic>Eczema</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lesions</topic><topic>Lymph nodes</topic><topic>MAP kinase</topic><topic>MAPK</topic><topic>NF-κB</topic><topic>NF-κB protein</topic><topic>Organs</topic><topic>Pathogenesis</topic><topic>Penicillin</topic><topic>Phosphorylation</topic><topic>Rumex japonicus Houtt</topic><topic>Skin</topic><topic>Skin diseases</topic><topic>skin lesion</topic><topic>Skin lesions</topic><topic>Spleen</topic><topic>TNF-α</topic><topic>Topical application</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Hye Ryeon</creatorcontrib><creatorcontrib>Lee, Hyunkyoung</creatorcontrib><creatorcontrib>Kim, Jong-Hyun</creatorcontrib><creatorcontrib>Hong, Il-Hwa</creatorcontrib><creatorcontrib>Hwang, Du Hyeon</creatorcontrib><creatorcontrib>Rho, Il Rae</creatorcontrib><creatorcontrib>Kim, Gon Sup</creatorcontrib><creatorcontrib>Kim, Euikyung</creatorcontrib><creatorcontrib>Kang, Changkeun</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nutrients</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Hye Ryeon</au><au>Lee, Hyunkyoung</au><au>Kim, Jong-Hyun</au><au>Hong, Il-Hwa</au><au>Hwang, Du Hyeon</au><au>Rho, Il Rae</au><au>Kim, Gon Sup</au><au>Kim, Euikyung</au><au>Kang, Changkeun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Therapeutic Effect of Rumex japonicus Houtt. on DNCB-Induced Atopic Dermatitis-Like Skin Lesions in Balb/c Mice and Human Keratinocyte HaCaT Cells</atitle><jtitle>Nutrients</jtitle><addtitle>Nutrients</addtitle><date>2019-03-07</date><risdate>2019</risdate><volume>11</volume><issue>3</issue><spage>573</spage><pages>573-</pages><issn>2072-6643</issn><eissn>2072-6643</eissn><abstract>Houtt. (RJ) is traditionally used in folk medicines to treat patients suffering from skin disease in Korea and other parts of East Asia. However, the beneficial effect of RJ extract on atopic dermatitis (AD) has not been thoroughly examined. Therefore, this study aimed to investigate the anti-inflammatory effects of RJ on AD in vitro and in vivo. Treatment with RJ inhibited the phosphorylation of mitogen-activated protein kinase (MAPK) as well as the activation of nuclear factor-kappa B (NF-κB) in tumor necrosis factor-α (TNF-α) stimulated in HaCaT cells. The five-week-old Balb/c mice were used as an AD-like mouse model by treating them with 1-chloro-2, 4-dinitrobenzene (DNCB). Topical administration of RJ to DNCB-treated mice significantly reduced clinical dermatitis severity, epidermal thickness, and decreased mast cell and eosinophil infiltration into skin and ear tissue. These results suggest that RJ inhibits the development of AD-like skin lesions by regulating the skin inflammation responses in HaCaT cells and Balb/c mice. Thus, RJ may be a potential therapeutic agent for AD.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>30866501</pmid><doi>10.3390/nu11030573</doi><orcidid>https://orcid.org/0000-0002-5114-5096</orcidid><orcidid>https://orcid.org/0000-0002-0844-1009</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | AKT protein Atopic dermatitis Cytokines Dermatitis DNCB Eczema Immune response Immune system Inflammation Kinases Laboratory animals Lesions Lymph nodes MAP kinase MAPK NF-κB NF-κB protein Organs Pathogenesis Penicillin Phosphorylation Rumex japonicus Houtt Skin Skin diseases skin lesion Skin lesions Spleen TNF-α Topical application Translocation |
title | Therapeutic Effect of Rumex japonicus Houtt. on DNCB-Induced Atopic Dermatitis-Like Skin Lesions in Balb/c Mice and Human Keratinocyte HaCaT Cells |
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