PoplarV1, Main, Exploration, bibRecord, 002062

Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.

Identifieur interne : 002062 ( Main/Exploration ); précédent : 002061; suivant : 002063

Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.

Auteurs : Dong-Joo Kwon [Corée du Sud] ; Young-Soo Bae [Corée du Sud] ; Sung Mi Ju [Corée du Sud] ; Gi Soo Youn [Corée du Sud] ; Soo Young Choi [Corée du Sud] ; Jinseu Park [Corée du Sud]

Source :

BMB reports [ 1976-670X ] ; 2014.

RBID : pubmed:24286322

Descripteurs français

KwdFr :
- Animaux (MeSH), Anti-inflammatoires (pharmacologie), Cytokines (métabolisme), Extraits de plantes (composition chimique), Extraits de plantes (pharmacologie), Facteur de transcription NF-kappa B (antagonistes et inhibiteurs), Facteur de transcription NF-kappa B (métabolisme), Facteur de transcription RelA (métabolisme), Glucosides (pharmacologie), Inhibiteur alpha de NF-KappaB (MeSH), JNK Mitogen-Activated Protein Kinases (métabolisme), Lignée cellulaire (MeSH), Lipopolysaccharides (toxicité), Macrophages (cytologie), Macrophages (effets des médicaments et des substances chimiques), Macrophages (métabolisme), Monoxyde d'azote (métabolisme), Nitric oxide synthase type II (métabolisme), Phosphorylation (effets des médicaments et des substances chimiques), Populus (métabolisme), Protéines I-kappa B (métabolisme), Souris (MeSH), Transduction du signal (effets des médicaments et des substances chimiques), Écorce (métabolisme).
MESH :
- antagonistes et inhibiteurs : Facteur de transcription NF-kappa B.
- composition chimique : Extraits de plantes.
- cytologie : Macrophages.
- effets des médicaments et des substances chimiques : Macrophages, Phosphorylation, Transduction du signal.
- métabolisme : Cytokines, Facteur de transcription NF-kappa B, Facteur de transcription RelA, JNK Mitogen-Activated Protein Kinases, Macrophages, Monoxyde d'azote, Nitric oxide synthase type II, Populus, Protéines I-kappa B, Écorce.
- pharmacologie : Anti-inflammatoires, Extraits de plantes, Glucosides.
- toxicité : Lipopolysaccharides.
- Animaux, Inhibiteur alpha de NF-KappaB, Lignée cellulaire, Souris.

English descriptors

KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (pharmacology), Cell Line (MeSH), Cytokines (metabolism), Glucosides (pharmacology), I-kappa B Proteins (metabolism), JNK Mitogen-Activated Protein Kinases (metabolism), Lipopolysaccharides (toxicity), Macrophages (cytology), Macrophages (drug effects), Macrophages (metabolism), Mice (MeSH), NF-KappaB Inhibitor alpha (MeSH), NF-kappa B (antagonists & inhibitors), NF-kappa B (metabolism), Nitric Oxide (metabolism), Nitric Oxide Synthase Type II (metabolism), Phosphorylation (drug effects), Plant Bark (metabolism), Plant Extracts (chemistry), Plant Extracts (pharmacology), Populus (metabolism), Signal Transduction (drug effects), Transcription Factor RelA (metabolism).
MESH :
- chemical , antagonists & inhibitors : NF-kappa B.
- chemical , chemistry : Plant Extracts.
- chemical , metabolism : Cytokines, I-kappa B Proteins, JNK Mitogen-Activated Protein Kinases, NF-kappa B, Nitric Oxide, Nitric Oxide Synthase Type II, Transcription Factor RelA.
- chemical , pharmacology : Anti-Inflammatory Agents, Glucosides, Plant Extracts.
- chemical , toxicity : Lipopolysaccharides.
- cytology : Macrophages.
- drug effects : Macrophages, Phosphorylation, Signal Transduction.
- metabolism : Macrophages, Plant Bark, Populus.
- Animals, Cell Line, Mice, NF-KappaB Inhibitor alpha.

Abstract

We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.

DOI: 10.5483/bmbrep.2014.47.6.200
PubMed: 24286322
PubMed Central: PMC4163874

Affiliations:

Corée du Sud

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 002393
to stream Main, to step Curation: 002393

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Cell Line (MeSH)</term>
<term>Cytokines (metabolism)</term>
<term>Glucosides (pharmacology)</term>
<term>I-kappa B Proteins (metabolism)</term>
<term>JNK Mitogen-Activated Protein Kinases (metabolism)</term>
<term>Lipopolysaccharides (toxicity)</term>
<term>Macrophages (cytology)</term>
<term>Macrophages (drug effects)</term>
<term>Macrophages (metabolism)</term>
<term>Mice (MeSH)</term>
<term>NF-KappaB Inhibitor alpha (MeSH)</term>
<term>NF-kappa B (antagonists & inhibitors)</term>
<term>NF-kappa B (metabolism)</term>
<term>Nitric Oxide (metabolism)</term>
<term>Nitric Oxide Synthase Type II (metabolism)</term>
<term>Phosphorylation (drug effects)</term>
<term>Plant Bark (metabolism)</term>
<term>Plant Extracts (chemistry)</term>
<term>Plant Extracts (pharmacology)</term>
<term>Populus (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Transcription Factor RelA (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Anti-inflammatoires (pharmacologie)</term>
<term>Cytokines (métabolisme)</term>
<term>Extraits de plantes (composition chimique)</term>
<term>Extraits de plantes (pharmacologie)</term>
<term>Facteur de transcription NF-kappa B (antagonistes et inhibiteurs)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur de transcription RelA (métabolisme)</term>
<term>Glucosides (pharmacologie)</term>
<term>Inhibiteur alpha de NF-KappaB (MeSH)</term>
<term>JNK Mitogen-Activated Protein Kinases (métabolisme)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lipopolysaccharides (toxicité)</term>
<term>Macrophages (cytologie)</term>
<term>Macrophages (effets des médicaments et des substances chimiques)</term>
<term>Macrophages (métabolisme)</term>
<term>Monoxyde d'azote (métabolisme)</term>
<term>Nitric oxide synthase type II (métabolisme)</term>
<term>Phosphorylation (effets des médicaments et des substances chimiques)</term>
<term>Populus (métabolisme)</term>
<term>Protéines I-kappa B (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Écorce (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>NF-kappa B</term>
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<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Plant Extracts</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>I-kappa B Proteins</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
<term>NF-kappa B</term>
<term>Nitric Oxide</term>
<term>Nitric Oxide Synthase Type II</term>
<term>Transcription Factor RelA</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Glucosides</term>
<term>Plant Extracts</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Lipopolysaccharides</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de transcription NF-kappa B</term>
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<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Extraits de plantes</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Macrophages</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Macrophages</term>
<term>Phosphorylation</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Macrophages</term>
<term>Phosphorylation</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Macrophages</term>
<term>Plant Bark</term>
<term>Populus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Facteur de transcription RelA</term>
<term>JNK Mitogen-Activated Protein Kinases</term>
<term>Macrophages</term>
<term>Monoxyde d'azote</term>
<term>Nitric oxide synthase type II</term>
<term>Populus</term>
<term>Protéines I-kappa B</term>
<term>Écorce</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term>
<term>Extraits de plantes</term>
<term>Glucosides</term>
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<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Lipopolysaccharides</term>
</keywords>
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<term>Cell Line</term>
<term>Mice</term>
<term>NF-KappaB Inhibitor alpha</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Inhibiteur alpha de NF-KappaB</term>
<term>Lignée cellulaire</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en">We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.</div>
</front>
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<Abstract><AbstractText>We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kwon</LastName>
<ForeName>Dong-Joo</ForeName>
<Initials>DJ</Initials>
<AffiliationInfo><Affiliation>Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702; Hongcheon Institute of Medicinal Herb, Hongcheon 200-930, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bae</LastName>
<ForeName>Young-Soo</ForeName>
<Initials>YS</Initials>
<AffiliationInfo><Affiliation>Department of Forest Biomaterials Engineering, Kangwon National University, Chuncheon 200-701, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ju</LastName>
<ForeName>Sung Mi</ForeName>
<Initials>SM</Initials>
<AffiliationInfo><Affiliation>Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Youn</LastName>
<ForeName>Gi Soo</ForeName>
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<AffiliationInfo><Affiliation>Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Choi</LastName>
<ForeName>Soo Young</ForeName>
<Initials>SY</Initials>
<AffiliationInfo><Affiliation>Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Park</LastName>
<ForeName>Jinseu</ForeName>
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<AffiliationInfo><Affiliation>Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.</Affiliation>
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   |texte=   Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.
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Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.

Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.

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