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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Veröffentlicht in:Inflammation 2020-02, Vol.43 (1), p.347-357
Hauptverfasser: Zhu, Tingting, Fang, Fumin, Sun, Dongjie, Yang, Shuyun, Zhang, Xiaoping, Yu, Xiuqin, Yang, Li
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container_start_page 347
container_title Inflammation
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creator Zhu, Tingting
Fang, Fumin
Sun, Dongjie
Yang, Shuyun
Zhang, Xiaoping
Yu, Xiuqin
Yang, Li
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.
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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. 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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 &amp; 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 ; 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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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