Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway
Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory an...
Gespeichert in:
| Veröffentlicht in: | International journal of molecular sciences 2024-12, Vol.25 (23), p.12737 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 23 |
| container_start_page | 12737 |
| container_title | International journal of molecular sciences |
| container_volume | 25 |
| creator | Shim, Ki-Shuk Kim, Hye Jin Ji, Kon-Young Jung, Dong Ho Park, Sun Haeng Song, Hyun-Kyung Kim, Taesoo Kim, Ki Mo |
| description | Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory and antioxidant properties. However, the effects of RA on
extract (DfE)-induced AD-like skin inflammation, as well as its ability to regulate oxidative stress through the Nrf2/HO-1 pathway in TNF-α/IFN-γ-treated keratinocytes, remain unclear. We investigated RA activity in a DfE-induced AD-like skin inflammation mouse model and IFN-γ/TNF-α-stimulated keratinocytes. We found that RA attenuates DfE-induced inflammation by decreasing dermatitis scores and serum inflammatory marker levels and mast cell infiltration. Additionally, RA significantly suppressed IFN-γ/TNF-α-induced chemokine production in keratinocytes and reduced Th cytokine levels in concanavalin A-stimulated splenocytes. Importantly, RA also increased Nrf2/HO-1 expression in TNF-α/IFN-γ-treated keratinocytes. In conclusion, this study demonstrated that RA effectively alleviates DfE-induced AD-like skin lesions by reducing the levels of inflammatory cytokines and chemokines. Furthermore, RA promotes Nrf2/HO-1 signaling in keratinocytes, which may help mitigate DfE-induced oxidative stress, thereby alleviating AD-like skin inflammation. These findings highlight the potential of RA as a therapeutic agent for treating AD and other skin inflammation. |
| doi_str_mv | 10.3390/ijms252312737 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_3146914703</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A819951497</galeid><sourcerecordid>A819951497</sourcerecordid><originalsourceid>FETCH-LOGICAL-c313t-6e9ba79c06c1a426241cceb076c13ff89b69b575cbc7ae458ba123fff8c6b74a3</originalsourceid><addsrcrecordid>eNptkk1v1DAQhiMEoh9w5IosceGS1l-J4-OqlHaliiIK58hxxrveJvZiO8D-Fv4sDltoi5AP9rx-3vHIM0XxiuATxiQ-tZsx0ooyQgUTT4pDwiktMa7F0wfng-Ioxg3GlNFKPi8OmKwbznl9WPz85OOognVWo4W2PVqMMFgfVIKI3kEYVfLbtVp522fBzKQCdP4jBaVTuXT9pCGbMpQT7HmbbCwHewvo5tY6tHRmUOOse4e6XX4l2W85ciuU1oA-BENPL69Lgm7syqlh1j-qtP6udi-KZ0YNEV7e7cfFl_fnn88uy6vri-XZ4qrUjLBU1iA7JaTGtSaK05pyojV0WOSYGdPIrpZdJSrdaaGAV02nCM0XptF1J7hix8Xbfd5t8F8niKkdbdQwDMqBn2LLCK8l4QKzjL75B934KeSyf1OcSCYZv6dWaoDWOuPn75qTtouGSFkRLkWmTv5D5dXDaLV3YGzWHxnKvUEHH2MA026Dzc3btQS38zC0j4Yh86_vip26Efq_9J_us1_3MrBi</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3144193934</pqid></control><display><type>article</type><title>Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway</title><source>MDPI - Multidisciplinary Digital Publishing Institute</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Shim, Ki-Shuk ; Kim, Hye Jin ; Ji, Kon-Young ; Jung, Dong Ho ; Park, Sun Haeng ; Song, Hyun-Kyung ; Kim, Taesoo ; Kim, Ki Mo</creator><creatorcontrib>Shim, Ki-Shuk ; Kim, Hye Jin ; Ji, Kon-Young ; Jung, Dong Ho ; Park, Sun Haeng ; Song, Hyun-Kyung ; Kim, Taesoo ; Kim, Ki Mo</creatorcontrib><description>Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory and antioxidant properties. However, the effects of RA on
extract (DfE)-induced AD-like skin inflammation, as well as its ability to regulate oxidative stress through the Nrf2/HO-1 pathway in TNF-α/IFN-γ-treated keratinocytes, remain unclear. We investigated RA activity in a DfE-induced AD-like skin inflammation mouse model and IFN-γ/TNF-α-stimulated keratinocytes. We found that RA attenuates DfE-induced inflammation by decreasing dermatitis scores and serum inflammatory marker levels and mast cell infiltration. Additionally, RA significantly suppressed IFN-γ/TNF-α-induced chemokine production in keratinocytes and reduced Th cytokine levels in concanavalin A-stimulated splenocytes. Importantly, RA also increased Nrf2/HO-1 expression in TNF-α/IFN-γ-treated keratinocytes. In conclusion, this study demonstrated that RA effectively alleviates DfE-induced AD-like skin lesions by reducing the levels of inflammatory cytokines and chemokines. Furthermore, RA promotes Nrf2/HO-1 signaling in keratinocytes, which may help mitigate DfE-induced oxidative stress, thereby alleviating AD-like skin inflammation. These findings highlight the potential of RA as a therapeutic agent for treating AD and other skin inflammation.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms252312737</identifier><identifier>PMID: 39684446</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acids ; Advertising executives ; Allergens ; Allergies ; Analysis ; Animals ; Anti-Inflammatory Agents - pharmacology ; Antigens, Dermatophagoides - immunology ; Antioxidants ; Atopic dermatitis ; B cells ; Cells ; Chemokines ; Cinnamates - pharmacology ; Cytokines ; Cytokines - metabolism ; Cytotoxicity ; Depsides - pharmacology ; Dermatitis ; Dermatitis, Atopic - chemically induced ; Dermatitis, Atopic - drug therapy ; Dermatitis, Atopic - metabolism ; Dermatitis, Atopic - pathology ; Dermatophagoides farinae - immunology ; Disease Models, Animal ; Heme Oxygenase-1 - metabolism ; Homeostasis ; Humans ; Immune response ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Inflammatory diseases ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Membrane Proteins ; Mice ; NF-E2-Related Factor 2 - metabolism ; Oxidative stress ; Oxidative Stress - drug effects ; Rosmarinic Acid ; Signal Transduction - drug effects ; Skin ; Skin - drug effects ; Skin - metabolism ; Skin - pathology ; Skin lesions ; Tumor necrosis factor ; Tumor necrosis factor-TNF</subject><ispartof>International journal of molecular sciences, 2024-12, Vol.25 (23), p.12737</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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 (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c313t-6e9ba79c06c1a426241cceb076c13ff89b69b575cbc7ae458ba123fff8c6b74a3</cites><orcidid>0000-0001-7104-8181 ; 0000-0001-7503-9725 ; 0000-0002-6250-5720 ; 0000-0002-9472-0724 ; 0000-0003-3992-8925</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39684446$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shim, Ki-Shuk</creatorcontrib><creatorcontrib>Kim, Hye Jin</creatorcontrib><creatorcontrib>Ji, Kon-Young</creatorcontrib><creatorcontrib>Jung, Dong Ho</creatorcontrib><creatorcontrib>Park, Sun Haeng</creatorcontrib><creatorcontrib>Song, Hyun-Kyung</creatorcontrib><creatorcontrib>Kim, Taesoo</creatorcontrib><creatorcontrib>Kim, Ki Mo</creatorcontrib><title>Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory and antioxidant properties. However, the effects of RA on
extract (DfE)-induced AD-like skin inflammation, as well as its ability to regulate oxidative stress through the Nrf2/HO-1 pathway in TNF-α/IFN-γ-treated keratinocytes, remain unclear. We investigated RA activity in a DfE-induced AD-like skin inflammation mouse model and IFN-γ/TNF-α-stimulated keratinocytes. We found that RA attenuates DfE-induced inflammation by decreasing dermatitis scores and serum inflammatory marker levels and mast cell infiltration. Additionally, RA significantly suppressed IFN-γ/TNF-α-induced chemokine production in keratinocytes and reduced Th cytokine levels in concanavalin A-stimulated splenocytes. Importantly, RA also increased Nrf2/HO-1 expression in TNF-α/IFN-γ-treated keratinocytes. In conclusion, this study demonstrated that RA effectively alleviates DfE-induced AD-like skin lesions by reducing the levels of inflammatory cytokines and chemokines. Furthermore, RA promotes Nrf2/HO-1 signaling in keratinocytes, which may help mitigate DfE-induced oxidative stress, thereby alleviating AD-like skin inflammation. These findings highlight the potential of RA as a therapeutic agent for treating AD and other skin inflammation.</description><subject>Acids</subject><subject>Advertising executives</subject><subject>Allergens</subject><subject>Allergies</subject><subject>Analysis</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antigens, Dermatophagoides - immunology</subject><subject>Antioxidants</subject><subject>Atopic dermatitis</subject><subject>B cells</subject><subject>Cells</subject><subject>Chemokines</subject><subject>Cinnamates - pharmacology</subject><subject>Cytokines</subject><subject>Cytokines - metabolism</subject><subject>Cytotoxicity</subject><subject>Depsides - pharmacology</subject><subject>Dermatitis</subject><subject>Dermatitis, Atopic - chemically induced</subject><subject>Dermatitis, Atopic - drug therapy</subject><subject>Dermatitis, Atopic - metabolism</subject><subject>Dermatitis, Atopic - pathology</subject><subject>Dermatophagoides farinae - immunology</subject><subject>Disease Models, Animal</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Immune response</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory diseases</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Rosmarinic Acid</subject><subject>Signal Transduction - drug effects</subject><subject>Skin</subject><subject>Skin - drug effects</subject><subject>Skin - metabolism</subject><subject>Skin - pathology</subject><subject>Skin lesions</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkk1v1DAQhiMEoh9w5IosceGS1l-J4-OqlHaliiIK58hxxrveJvZiO8D-Fv4sDltoi5AP9rx-3vHIM0XxiuATxiQ-tZsx0ooyQgUTT4pDwiktMa7F0wfng-Ioxg3GlNFKPi8OmKwbznl9WPz85OOognVWo4W2PVqMMFgfVIKI3kEYVfLbtVp522fBzKQCdP4jBaVTuXT9pCGbMpQT7HmbbCwHewvo5tY6tHRmUOOse4e6XX4l2W85ciuU1oA-BENPL69Lgm7syqlh1j-qtP6udi-KZ0YNEV7e7cfFl_fnn88uy6vri-XZ4qrUjLBU1iA7JaTGtSaK05pyojV0WOSYGdPIrpZdJSrdaaGAV02nCM0XptF1J7hix8Xbfd5t8F8niKkdbdQwDMqBn2LLCK8l4QKzjL75B934KeSyf1OcSCYZv6dWaoDWOuPn75qTtouGSFkRLkWmTv5D5dXDaLV3YGzWHxnKvUEHH2MA026Dzc3btQS38zC0j4Yh86_vip26Efq_9J_us1_3MrBi</recordid><startdate>20241201</startdate><enddate>20241201</enddate><creator>Shim, Ki-Shuk</creator><creator>Kim, Hye Jin</creator><creator>Ji, Kon-Young</creator><creator>Jung, Dong Ho</creator><creator>Park, Sun Haeng</creator><creator>Song, Hyun-Kyung</creator><creator>Kim, Taesoo</creator><creator>Kim, Ki Mo</creator><general>MDPI AG</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7104-8181</orcidid><orcidid>https://orcid.org/0000-0001-7503-9725</orcidid><orcidid>https://orcid.org/0000-0002-6250-5720</orcidid><orcidid>https://orcid.org/0000-0002-9472-0724</orcidid><orcidid>https://orcid.org/0000-0003-3992-8925</orcidid></search><sort><creationdate>20241201</creationdate><title>Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway</title><author>Shim, Ki-Shuk ; Kim, Hye Jin ; Ji, Kon-Young ; Jung, Dong Ho ; Park, Sun Haeng ; Song, Hyun-Kyung ; Kim, Taesoo ; Kim, Ki Mo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c313t-6e9ba79c06c1a426241cceb076c13ff89b69b575cbc7ae458ba123fff8c6b74a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acids</topic><topic>Advertising executives</topic><topic>Allergens</topic><topic>Allergies</topic><topic>Analysis</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antigens, Dermatophagoides - immunology</topic><topic>Antioxidants</topic><topic>Atopic dermatitis</topic><topic>B cells</topic><topic>Cells</topic><topic>Chemokines</topic><topic>Cinnamates - pharmacology</topic><topic>Cytokines</topic><topic>Cytokines - metabolism</topic><topic>Cytotoxicity</topic><topic>Depsides - pharmacology</topic><topic>Dermatitis</topic><topic>Dermatitis, Atopic - chemically induced</topic><topic>Dermatitis, Atopic - drug therapy</topic><topic>Dermatitis, Atopic - metabolism</topic><topic>Dermatitis, Atopic - pathology</topic><topic>Dermatophagoides farinae - immunology</topic><topic>Disease Models, Animal</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Immune response</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory diseases</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Membrane Proteins</topic><topic>Mice</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Rosmarinic Acid</topic><topic>Signal Transduction - drug effects</topic><topic>Skin</topic><topic>Skin - drug effects</topic><topic>Skin - metabolism</topic><topic>Skin - pathology</topic><topic>Skin lesions</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shim, Ki-Shuk</creatorcontrib><creatorcontrib>Kim, Hye Jin</creatorcontrib><creatorcontrib>Ji, Kon-Young</creatorcontrib><creatorcontrib>Jung, Dong Ho</creatorcontrib><creatorcontrib>Park, Sun Haeng</creatorcontrib><creatorcontrib>Song, Hyun-Kyung</creatorcontrib><creatorcontrib>Kim, Taesoo</creatorcontrib><creatorcontrib>Kim, Ki Mo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</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 Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shim, Ki-Shuk</au><au>Kim, Hye Jin</au><au>Ji, Kon-Young</au><au>Jung, Dong Ho</au><au>Park, Sun Haeng</au><au>Song, Hyun-Kyung</au><au>Kim, Taesoo</au><au>Kim, Ki Mo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-12-01</date><risdate>2024</risdate><volume>25</volume><issue>23</issue><spage>12737</spage><pages>12737-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases. AD pathogenesis is associated with increased oxidative stress, impairment of the skin barrier, and activation of the immune response. Rosmarinic acid (RA), a caffeic acid ester, is known for its anti-inflammatory and antioxidant properties. However, the effects of RA on
extract (DfE)-induced AD-like skin inflammation, as well as its ability to regulate oxidative stress through the Nrf2/HO-1 pathway in TNF-α/IFN-γ-treated keratinocytes, remain unclear. We investigated RA activity in a DfE-induced AD-like skin inflammation mouse model and IFN-γ/TNF-α-stimulated keratinocytes. We found that RA attenuates DfE-induced inflammation by decreasing dermatitis scores and serum inflammatory marker levels and mast cell infiltration. Additionally, RA significantly suppressed IFN-γ/TNF-α-induced chemokine production in keratinocytes and reduced Th cytokine levels in concanavalin A-stimulated splenocytes. Importantly, RA also increased Nrf2/HO-1 expression in TNF-α/IFN-γ-treated keratinocytes. In conclusion, this study demonstrated that RA effectively alleviates DfE-induced AD-like skin lesions by reducing the levels of inflammatory cytokines and chemokines. Furthermore, RA promotes Nrf2/HO-1 signaling in keratinocytes, which may help mitigate DfE-induced oxidative stress, thereby alleviating AD-like skin inflammation. These findings highlight the potential of RA as a therapeutic agent for treating AD and other skin inflammation.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39684446</pmid><doi>10.3390/ijms252312737</doi><orcidid>https://orcid.org/0000-0001-7104-8181</orcidid><orcidid>https://orcid.org/0000-0001-7503-9725</orcidid><orcidid>https://orcid.org/0000-0002-6250-5720</orcidid><orcidid>https://orcid.org/0000-0002-9472-0724</orcidid><orcidid>https://orcid.org/0000-0003-3992-8925</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2024-12, Vol.25 (23), p.12737 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3146914703 |
| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Acids Advertising executives Allergens Allergies Analysis Animals Anti-Inflammatory Agents - pharmacology Antigens, Dermatophagoides - immunology Antioxidants Atopic dermatitis B cells Cells Chemokines Cinnamates - pharmacology Cytokines Cytokines - metabolism Cytotoxicity Depsides - pharmacology Dermatitis Dermatitis, Atopic - chemically induced Dermatitis, Atopic - drug therapy Dermatitis, Atopic - metabolism Dermatitis, Atopic - pathology Dermatophagoides farinae - immunology Disease Models, Animal Heme Oxygenase-1 - metabolism Homeostasis Humans Immune response Inflammation Inflammation - drug therapy Inflammation - metabolism Inflammatory diseases Keratinocytes - drug effects Keratinocytes - metabolism Membrane Proteins Mice NF-E2-Related Factor 2 - metabolism Oxidative stress Oxidative Stress - drug effects Rosmarinic Acid Signal Transduction - drug effects Skin Skin - drug effects Skin - metabolism Skin - pathology Skin lesions Tumor necrosis factor Tumor necrosis factor-TNF |
| title | Rosmarinic Acid Ameliorates Dermatophagoides farinae Extract-Induced Atopic Dermatitis-like Skin Inflammation by Activating the Nrf2/HO-1 Signaling Pathway |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T16%3A49%3A57IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Rosmarinic%20Acid%20Ameliorates%20Dermatophagoides%20farinae%20Extract-Induced%20Atopic%20Dermatitis-like%20Skin%20Inflammation%20by%20Activating%20the%20Nrf2/HO-1%20Signaling%20Pathway&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Shim,%20Ki-Shuk&rft.date=2024-12-01&rft.volume=25&rft.issue=23&rft.spage=12737&rft.pages=12737-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms252312737&rft_dat=%3Cgale_proqu%3EA819951497%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3144193934&rft_id=info:pmid/39684446&rft_galeid=A819951497&rfr_iscdi=true |