Anti-Inflammatory Activity of Populus deltoides Leaf Extract via Modulating NF-κB and p38/JNK Pathways.
Identifieur interne : 001049 ( Main/Exploration ); précédent : 001048; suivant : 001050Anti-Inflammatory Activity of Populus deltoides Leaf Extract via Modulating NF-κB and p38/JNK Pathways.
Auteurs : Ye Eun Jeong [Corée du Sud] ; Mi-Young Lee [Corée du Sud]Source :
- International journal of molecular sciences [ 1422-0067 ] ; 2018.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anti-inflammatoires (isolement et purification), Anti-inflammatoires (pharmacologie), Cellules RAW 264.7 (MeSH), Cyclooxygenase 2 (pharmacologie), Dinoprostone (pharmacologie), Extraits de plantes (composition chimique), Facteur de nécrose tumorale alpha (génétique), Facteur de nécrose tumorale alpha (métabolisme), Facteur de transcription NF-kappa B (génétique), Facteur de transcription NF-kappa B (métabolisme), Feuilles de plante (composition chimique), Inhibiteur alpha de NF-KappaB (génétique), Inhibiteur alpha de NF-KappaB (métabolisme), Lipopolysaccharides (antagonistes et inhibiteurs), Lipopolysaccharides (pharmacologie), MAP Kinase Kinase 4 (génétique), MAP Kinase Kinase 4 (métabolisme), Monoxyde d'azote (antagonistes et inhibiteurs), Monoxyde d'azote (biosynthèse), Nitric oxide synthase type II (génétique), Nitric oxide synthase type II (métabolisme), Phosphorylation (effets des médicaments et des substances chimiques), Populus (composition chimique), Régulation de l'expression des gènes (MeSH), Souris (MeSH), Survie cellulaire (effets des médicaments et des substances chimiques), Transduction du signal (MeSH), p38 Mitogen-Activated Protein Kinases (génétique), p38 Mitogen-Activated Protein Kinases (métabolisme).
- MESH :
- antagonistes et inhibiteurs : Lipopolysaccharides, Monoxyde d'azote.
- biosynthèse : Monoxyde d'azote.
- composition chimique : Extraits de plantes, Feuilles de plante, Populus.
- effets des médicaments et des substances chimiques : Phosphorylation, Survie cellulaire.
- génétique : Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Inhibiteur alpha de NF-KappaB, MAP Kinase Kinase 4, Nitric oxide synthase type II, p38 Mitogen-Activated Protein Kinases.
- isolement et purification : Anti-inflammatoires.
- métabolisme : Facteur de nécrose tumorale alpha, Facteur de transcription NF-kappa B, Inhibiteur alpha de NF-KappaB, MAP Kinase Kinase 4, Nitric oxide synthase type II, p38 Mitogen-Activated Protein Kinases.
- pharmacologie : Anti-inflammatoires, Cyclooxygenase 2, Dinoprostone, Lipopolysaccharides.
- Animaux, Cellules RAW 264.7, Régulation de l'expression des gènes, Souris, Transduction du signal.
English descriptors
- KwdEn :
- Animals (MeSH), Anti-Inflammatory Agents (isolation & purification), Anti-Inflammatory Agents (pharmacology), Cell Survival (drug effects), Cyclooxygenase 2 (pharmacology), Dinoprostone (pharmacology), Gene Expression Regulation (MeSH), Lipopolysaccharides (antagonists & inhibitors), Lipopolysaccharides (pharmacology), MAP Kinase Kinase 4 (genetics), MAP Kinase Kinase 4 (metabolism), Mice (MeSH), NF-KappaB Inhibitor alpha (genetics), NF-KappaB Inhibitor alpha (metabolism), NF-kappa B (genetics), NF-kappa B (metabolism), Nitric Oxide (antagonists & inhibitors), Nitric Oxide (biosynthesis), Nitric Oxide Synthase Type II (genetics), Nitric Oxide Synthase Type II (metabolism), Phosphorylation (drug effects), Plant Extracts (chemistry), Plant Leaves (chemistry), Populus (chemistry), RAW 264.7 Cells (MeSH), Signal Transduction (MeSH), Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism), p38 Mitogen-Activated Protein Kinases (genetics), p38 Mitogen-Activated Protein Kinases (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Lipopolysaccharides, Nitric Oxide.
- chemical , biosynthesis : Nitric Oxide.
- chemical , chemistry : Plant Extracts.
- chemical , genetics : MAP Kinase Kinase 4, NF-KappaB Inhibitor alpha, NF-kappa B, Nitric Oxide Synthase Type II, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
- chemical , isolation & purification : Anti-Inflammatory Agents.
- chemical , metabolism : MAP Kinase Kinase 4, NF-KappaB Inhibitor alpha, NF-kappa B, Nitric Oxide Synthase Type II, Tumor Necrosis Factor-alpha, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Anti-Inflammatory Agents, Cyclooxygenase 2, Dinoprostone, Lipopolysaccharides.
- chemistry : Plant Leaves, Populus.
- drug effects : Cell Survival, Phosphorylation.
- Animals, Gene Expression Regulation, Mice, RAW 264.7 Cells, Signal Transduction.
Abstract
Populus deltoides, known as eastern cottonwood, has been commonly used as a medicinal plant. The aim of the present study was to investigate the mechanism underlying the anti-inflammatory activity of P. deltoides leaf extract (PLE). PLE effectively inhibited the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, but not that of cyclooxygenase-2 (COX-2) and prostaglandin E2. Proinflammatory tumor necrosis factor alpha (TNF-α) levels were also reduced by the extract. PLE inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and inhibitor of Kappa Bα (IκBα), and blunted LPS-triggered enhanced nuclear translocation of NF-κB p65. In mitogen-activated protein kinase (MAPK) signaling, PLE effectively decreased the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK), but not of extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these results suggest that anti-inflammatory activity of P. deltoides leaf extract might be driven by iNOS and NO inhibition mediated by modulation of the NF-κB and p38/JNK signaling pathways.
DOI: 10.3390/ijms19123746
PubMed: 30477268
PubMed Central: PMC6320835
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Cell Survival (drug effects)</term>
<term>Cyclooxygenase 2 (pharmacology)</term>
<term>Dinoprostone (pharmacology)</term>
<term>Gene Expression Regulation (MeSH)</term>
<term>Lipopolysaccharides (antagonists & inhibitors)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>MAP Kinase Kinase 4 (genetics)</term>
<term>MAP Kinase Kinase 4 (metabolism)</term>
<term>Mice (MeSH)</term>
<term>NF-KappaB Inhibitor alpha (genetics)</term>
<term>NF-KappaB Inhibitor alpha (metabolism)</term>
<term>NF-kappa B (genetics)</term>
<term>NF-kappa B (metabolism)</term>
<term>Nitric Oxide (antagonists & inhibitors)</term>
<term>Nitric Oxide (biosynthesis)</term>
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<term>Nitric Oxide Synthase Type II (metabolism)</term>
<term>Phosphorylation (drug effects)</term>
<term>Plant Extracts (chemistry)</term>
<term>Plant Leaves (chemistry)</term>
<term>Populus (chemistry)</term>
<term>RAW 264.7 Cells (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
<term>Tumor Necrosis Factor-alpha (genetics)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
<term>p38 Mitogen-Activated Protein Kinases (genetics)</term>
<term>p38 Mitogen-Activated Protein Kinases (metabolism)</term>
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<term>Anti-inflammatoires (isolement et purification)</term>
<term>Anti-inflammatoires (pharmacologie)</term>
<term>Cellules RAW 264.7 (MeSH)</term>
<term>Cyclooxygenase 2 (pharmacologie)</term>
<term>Dinoprostone (pharmacologie)</term>
<term>Extraits de plantes (composition chimique)</term>
<term>Facteur de nécrose tumorale alpha (génétique)</term>
<term>Facteur de nécrose tumorale alpha (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (génétique)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Feuilles de plante (composition chimique)</term>
<term>Inhibiteur alpha de NF-KappaB (génétique)</term>
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<term>Lipopolysaccharides (antagonistes et inhibiteurs)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>MAP Kinase Kinase 4 (génétique)</term>
<term>MAP Kinase Kinase 4 (métabolisme)</term>
<term>Monoxyde d'azote (antagonistes et inhibiteurs)</term>
<term>Monoxyde d'azote (biosynthèse)</term>
<term>Nitric oxide synthase type II (génétique)</term>
<term>Nitric oxide synthase type II (métabolisme)</term>
<term>Phosphorylation (effets des médicaments et des substances chimiques)</term>
<term>Populus (composition chimique)</term>
<term>Régulation de l'expression des gènes (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Survie cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (MeSH)</term>
<term>p38 Mitogen-Activated Protein Kinases (génétique)</term>
<term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term>
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<term>Nitric Oxide</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Nitric Oxide</term>
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<term>NF-KappaB Inhibitor alpha</term>
<term>NF-kappa B</term>
<term>Nitric Oxide Synthase Type II</term>
<term>Tumor Necrosis Factor-alpha</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>NF-KappaB Inhibitor alpha</term>
<term>NF-kappa B</term>
<term>Nitric Oxide Synthase Type II</term>
<term>Tumor Necrosis Factor-alpha</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Dinoprostone</term>
<term>Lipopolysaccharides</term>
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<term>Monoxyde d'azote</term>
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</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Plant Leaves</term>
<term>Populus</term>
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<keywords scheme="MESH" qualifier="composition chimique" xml:lang="fr"><term>Extraits de plantes</term>
<term>Feuilles de plante</term>
<term>Populus</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Survival</term>
<term>Phosphorylation</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Phosphorylation</term>
<term>Survie cellulaire</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Inhibiteur alpha de NF-KappaB</term>
<term>MAP Kinase Kinase 4</term>
<term>Nitric oxide synthase type II</term>
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<keywords scheme="MESH" qualifier="isolement et purification" xml:lang="fr"><term>Anti-inflammatoires</term>
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<term>MAP Kinase Kinase 4</term>
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<term>Dinoprostone</term>
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<term>Gene Expression Regulation</term>
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<term>RAW 264.7 Cells</term>
<term>Signal Transduction</term>
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<term>Cellules RAW 264.7</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en"><i>Populus deltoides</i>
, known as eastern cottonwood, has been commonly used as a medicinal plant. The aim of the present study was to investigate the mechanism underlying the anti-inflammatory activity of <i>P. deltoides</i>
leaf extract (PLE). PLE effectively inhibited the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, but not that of cyclooxygenase-2 (COX-2) and prostaglandin E2. Proinflammatory tumor necrosis factor alpha (TNF-α) levels were also reduced by the extract. PLE inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and inhibitor of Kappa Bα (IκBα), and blunted LPS-triggered enhanced nuclear translocation of NF-κB p65. In mitogen-activated protein kinase (MAPK) signaling, PLE effectively decreased the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK), but not of extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these results suggest that anti-inflammatory activity of <i>P. deltoides</i>
leaf extract might be driven by iNOS and NO inhibition mediated by modulation of the NF-κB and p38/JNK signaling pathways.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30477268</PMID>
<DateCompleted><Year>2019</Year>
<Month>03</Month>
<Day>08</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
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<Month>Nov</Month>
<Day>25</Day>
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<Title>International journal of molecular sciences</Title>
<ISOAbbreviation>Int J Mol Sci</ISOAbbreviation>
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<ArticleTitle>Anti-Inflammatory Activity of <i>Populus deltoides</i>
Leaf Extract via Modulating NF-κB and p38/JNK Pathways.</ArticleTitle>
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<Abstract><AbstractText><i>Populus deltoides</i>
, known as eastern cottonwood, has been commonly used as a medicinal plant. The aim of the present study was to investigate the mechanism underlying the anti-inflammatory activity of <i>P. deltoides</i>
leaf extract (PLE). PLE effectively inhibited the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, but not that of cyclooxygenase-2 (COX-2) and prostaglandin E2. Proinflammatory tumor necrosis factor alpha (TNF-α) levels were also reduced by the extract. PLE inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and inhibitor of Kappa Bα (IκBα), and blunted LPS-triggered enhanced nuclear translocation of NF-κB p65. In mitogen-activated protein kinase (MAPK) signaling, PLE effectively decreased the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK), but not of extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these results suggest that anti-inflammatory activity of <i>P. deltoides</i>
leaf extract might be driven by iNOS and NO inhibition mediated by modulation of the NF-κB and p38/JNK signaling pathways.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jeong</LastName>
<ForeName>Ye Eun</ForeName>
<Initials>YE</Initials>
<AffiliationInfo><Affiliation>Department of Medical Science, College of Medical Science, Soonchunhyang University, Asan, Chungnam 31538, Korea. jye0564@naver.com.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Mi-Young</ForeName>
<Initials>MY</Initials>
<Identifier Source="ORCID">0000-0003-3511-9522</Identifier>
<AffiliationInfo><Affiliation>Department of Medical Biotechnology, College of Medical Science, Soonchunhyang University, Asan, Chungnam 31538, Korea. miyoung@sch.ac.kr.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>11</Month>
<Day>25</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>Switzerland</Country>
<MedlineTA>Int J Mol Sci</MedlineTA>
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<MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName>
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<MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName>
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<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D048670" MajorTopicYN="N">MAP Kinase Kinase 4</DescriptorName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
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<MeshHeading><DescriptorName UI="D000072000" MajorTopicYN="N">NF-KappaB Inhibitor alpha</DescriptorName>
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