Piceatannol Inhibits P. acnes–Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response
The Cutibacterium acnes (also called Propionibacterium acnes , P. acnes )-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3′, 4′-tetrahydroxy-tran...
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description | The
Cutibacterium acnes
(also called
Propionibacterium acnes
,
P. acnes
)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3′, 4′-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in
P. acnes
-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited
P. acnes
-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited
P. acnes
-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated
P. acnes
-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV. |
doi_str_mv | 10.1007/s10753-019-01125-8 |
format | Article |
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Cutibacterium acnes
(also called
Propionibacterium acnes
,
P. acnes
)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3′, 4′-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in
P. acnes
-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited
P. acnes
-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited
P. acnes
-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated
P. acnes
-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-019-01125-8</identifier><identifier>PMID: 31728743</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acne ; Acne Vulgaris - metabolism ; Acne Vulgaris - microbiology ; Acne Vulgaris - pathology ; Acne Vulgaris - prevention & control ; Anti-Inflammatory Agents - pharmacology ; Antioxidants ; Antioxidants - pharmacology ; Biomedical and Life Sciences ; Biomedicine ; Cell growth ; Cell Line ; Cell Movement - drug effects ; Cell proliferation ; Cell Proliferation - drug effects ; Cytokines ; Host-Pathogen Interactions ; Humans ; Immunology ; Inflammation Mediators - metabolism ; Interleukin 6 ; Interleukin 8 ; Internal Medicine ; Keratinocytes ; Keratinocytes - drug effects ; Keratinocytes - metabolism ; Keratinocytes - microbiology ; Keratinocytes - pathology ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; NF-κB protein ; Nuclear transport ; Original Article ; Oxidative stress ; Oxidative Stress - drug effects ; Pathology ; Pharmacology/Toxicology ; Piceatannol ; Propionibacterium acnes - pathogenicity ; Reactive oxygen species ; Rheumatology ; Signal Transduction ; Skin - drug effects ; Skin - metabolism ; Skin - microbiology ; Skin - pathology ; Skin diseases ; Stilbenes - pharmacology ; Toxicity ; trans-Stilbene ; Transcription Factor RelA - genetics ; Transcription Factor RelA - metabolism ; Transfection ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Tumors</subject><ispartof>Inflammation, 2020-02, Vol.43 (1), p.347-357</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Inflammation is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-a94c40c5c03e22f5332316db059e5acd48f14812c38aaa3354e888ff2d0fc9563</citedby><cites>FETCH-LOGICAL-c375t-a94c40c5c03e22f5332316db059e5acd48f14812c38aaa3354e888ff2d0fc9563</cites><orcidid>0000-0003-0951-6209</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10753-019-01125-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-019-01125-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31728743$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Tingting</creatorcontrib><creatorcontrib>Fang, Fumin</creatorcontrib><creatorcontrib>Sun, Dongjie</creatorcontrib><creatorcontrib>Yang, Shuyun</creatorcontrib><creatorcontrib>Zhang, Xiaoping</creatorcontrib><creatorcontrib>Yu, Xiuqin</creatorcontrib><creatorcontrib>Yang, Li</creatorcontrib><title>Piceatannol Inhibits P. acnes–Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>The
Cutibacterium acnes
(also called
Propionibacterium acnes
,
P. acnes
)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3′, 4′-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in
P. acnes
-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited
P. acnes
-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited
P. acnes
-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated
P. acnes
-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV.</description><subject>Acne</subject><subject>Acne Vulgaris - metabolism</subject><subject>Acne Vulgaris - microbiology</subject><subject>Acne Vulgaris - pathology</subject><subject>Acne Vulgaris - prevention & control</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Antioxidants</subject><subject>Antioxidants - pharmacology</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell growth</subject><subject>Cell Line</subject><subject>Cell Movement - drug effects</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Cytokines</subject><subject>Host-Pathogen Interactions</subject><subject>Humans</subject><subject>Immunology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Interleukin 6</subject><subject>Interleukin 8</subject><subject>Internal Medicine</subject><subject>Keratinocytes</subject><subject>Keratinocytes - drug effects</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - microbiology</subject><subject>Keratinocytes - pathology</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathology</subject><subject>Pharmacology/Toxicology</subject><subject>Piceatannol</subject><subject>Propionibacterium acnes - pathogenicity</subject><subject>Reactive oxygen species</subject><subject>Rheumatology</subject><subject>Signal Transduction</subject><subject>Skin - drug effects</subject><subject>Skin - metabolism</subject><subject>Skin - microbiology</subject><subject>Skin - pathology</subject><subject>Skin diseases</subject><subject>Stilbenes - pharmacology</subject><subject>Toxicity</subject><subject>trans-Stilbene</subject><subject>Transcription Factor RelA - genetics</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Transfection</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9Uc1u1DAQthAV3ba8AAdkiXOK7YkT54gKLasWdQXlbHmd8TZV1l5sh3ZvvELFG_Ikzf4Ubhys8cx8P9J8hLzh7JQzVr9PnNUSCsab8XEhC_WCTLisoRCyrl6SCYOKFdA09SE5SumOMaYaBa_IIfBaqLqECXmcdRZNNt6Hnk79bTfvcqKzU2qsx_Tn1--pbweLLb3EaHLng11npLMY-s5tJ8FT41v6pVvsu_mafgz3PuJi6DeMBb1-6Nrx9xPptxwxpS0h3-Lo53qzXJoc4pp-xbQKPuEJOXCmT_h6X4_J9_NPN2efi6vri-nZh6vCQi1zYZrSlsxKywCFcBJAAK_aOZMNSmPbUjleKi4sKGMMgCxRKeWcaJmzjazgmLzb6a5i-DFgyvouDNGPllqA5JzJim1QYoeyMaQU0elV7JYmrjVnepOC3qWgxxT0NgWtRtLbvfQwX2L7l_J89hEAO0AaV36B8Z_3f2SfAEjnlfs</recordid><startdate>20200201</startdate><enddate>20200201</enddate><creator>Zhu, Tingting</creator><creator>Fang, Fumin</creator><creator>Sun, Dongjie</creator><creator>Yang, Shuyun</creator><creator>Zhang, Xiaoping</creator><creator>Yu, Xiuqin</creator><creator>Yang, Li</creator><general>Springer US</general><general>Springer Nature B.V</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>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-0951-6209</orcidid></search><sort><creationdate>20200201</creationdate><title>Piceatannol Inhibits P. acnes–Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response</title><author>Zhu, Tingting ; Fang, Fumin ; Sun, Dongjie ; Yang, Shuyun ; Zhang, Xiaoping ; Yu, Xiuqin ; Yang, Li</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-a94c40c5c03e22f5332316db059e5acd48f14812c38aaa3354e888ff2d0fc9563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acne</topic><topic>Acne Vulgaris - metabolism</topic><topic>Acne Vulgaris - microbiology</topic><topic>Acne Vulgaris - pathology</topic><topic>Acne Vulgaris - prevention & control</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Antioxidants</topic><topic>Antioxidants - pharmacology</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell growth</topic><topic>Cell Line</topic><topic>Cell Movement - drug effects</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Cytokines</topic><topic>Host-Pathogen Interactions</topic><topic>Humans</topic><topic>Immunology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Interleukin 6</topic><topic>Interleukin 8</topic><topic>Internal Medicine</topic><topic>Keratinocytes</topic><topic>Keratinocytes - drug effects</topic><topic>Keratinocytes - metabolism</topic><topic>Keratinocytes - microbiology</topic><topic>Keratinocytes - pathology</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>NF-κB protein</topic><topic>Nuclear transport</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pathology</topic><topic>Pharmacology/Toxicology</topic><topic>Piceatannol</topic><topic>Propionibacterium acnes - pathogenicity</topic><topic>Reactive oxygen species</topic><topic>Rheumatology</topic><topic>Signal Transduction</topic><topic>Skin - drug effects</topic><topic>Skin - metabolism</topic><topic>Skin - microbiology</topic><topic>Skin - pathology</topic><topic>Skin diseases</topic><topic>Stilbenes - pharmacology</topic><topic>Toxicity</topic><topic>trans-Stilbene</topic><topic>Transcription Factor RelA - genetics</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Transfection</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Tingting</creatorcontrib><creatorcontrib>Fang, Fumin</creatorcontrib><creatorcontrib>Sun, Dongjie</creatorcontrib><creatorcontrib>Yang, Shuyun</creatorcontrib><creatorcontrib>Zhang, Xiaoping</creatorcontrib><creatorcontrib>Yu, Xiuqin</creatorcontrib><creatorcontrib>Yang, Li</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>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Tingting</au><au>Fang, Fumin</au><au>Sun, Dongjie</au><au>Yang, Shuyun</au><au>Zhang, Xiaoping</au><au>Yu, Xiuqin</au><au>Yang, Li</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Piceatannol Inhibits P. acnes–Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2020-02-01</date><risdate>2020</risdate><volume>43</volume><issue>1</issue><spage>347</spage><epage>357</epage><pages>347-357</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>The
Cutibacterium acnes
(also called
Propionibacterium acnes
,
P. acnes
)-induced proliferation and migration of keratinocytes contribute to acne vulgaris (AV), which is a common inflammatory skin disease that causes physical and psychological impairments. Piceatannol (3, 5, 3′, 4′-tetrahydroxy-trans-stilbene, PCT) is naturally present in many human diets and plays antioxidant and anti-inflammatory roles that inhibit cell proliferation and migration. We aimed to analyse the functions and underlying mechanisms of PCT in
P. acnes
-stimulated keratinocytes. First, PCT showed no toxicity against the normal human keratinocyte cell line HaCaT but inhibited
P. acnes
-induced HaCaT cell proliferation. Next, PCT promoted the nuclear translocation and target gene transcription of the antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), thereafter decreasing intracellular reactive oxygen species (ROS) levels. In addition, PCT inhibited the nuclear translocation of p65 [a subunit of nuclear factor kappa B (NF-κB)] and the secretion of pro-inflammatory cytokines, including interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8). Finally, a transfection assay showed that PCT inhibited
P. acnes
-induced HaCaT cell proliferation and migration by activating the antioxidant Nrf2 pathway and inhibiting the inflammatory NF-κB pathway. Our data suggested that PCT alleviated
P. acnes
-induced HaCaT cell proliferation and migration through its antioxidant and anti-inflammatory roles, suggesting the potential of PCT to treat AV.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31728743</pmid><doi>10.1007/s10753-019-01125-8</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0003-0951-6209</orcidid></addata></record> |
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subjects | Acne Acne Vulgaris - metabolism Acne Vulgaris - microbiology Acne Vulgaris - pathology Acne Vulgaris - prevention & control Anti-Inflammatory Agents - pharmacology Antioxidants Antioxidants - pharmacology Biomedical and Life Sciences Biomedicine Cell growth Cell Line Cell Movement - drug effects Cell proliferation Cell Proliferation - drug effects Cytokines Host-Pathogen Interactions Humans Immunology Inflammation Mediators - metabolism Interleukin 6 Interleukin 8 Internal Medicine Keratinocytes Keratinocytes - drug effects Keratinocytes - metabolism Keratinocytes - microbiology Keratinocytes - pathology NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism NF-κB protein Nuclear transport Original Article Oxidative stress Oxidative Stress - drug effects Pathology Pharmacology/Toxicology Piceatannol Propionibacterium acnes - pathogenicity Reactive oxygen species Rheumatology Signal Transduction Skin - drug effects Skin - metabolism Skin - microbiology Skin - pathology Skin diseases Stilbenes - pharmacology Toxicity trans-Stilbene Transcription Factor RelA - genetics Transcription Factor RelA - metabolism Transfection Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors |
title | Piceatannol Inhibits P. acnes–Induced Keratinocyte Proliferation and Migration by Downregulating Oxidative Stress and the Inflammatory Response |
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