PoplarV1, Main, Exploration, bibRecord, 000B26

Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.

Identifieur interne : 000B26 ( Main/Exploration ); précédent : 000B25; suivant : 000B27

Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.

Auteurs : Hongzhuan Xuan [République populaire de Chine] ; Wenwen Yuan [République populaire de Chine] ; Huasong Chang [République populaire de Chine] ; Minmin Liu [République populaire de Chine] ; Fuliang Hu [République populaire de Chine]

Source :

Inflammopharmacology [ 1568-5608 ] ; 2019.

RBID : pubmed:30251233

Descripteurs français

English descriptors

KwdEn :
- Anti-Inflammatory Agents (pharmacology), Autophagy (drug effects), Cell Line (MeSH), Cell Proliferation (drug effects), Human Umbilical Vein Endothelial Cells (drug effects), Human Umbilical Vein Endothelial Cells (metabolism), Humans (MeSH), Inflammation (drug therapy), Inflammation (metabolism), Lipopolysaccharides (pharmacology), MAP Kinase Signaling System (drug effects), Membrane Potential, Mitochondrial (drug effects), NF-kappa B (metabolism), Propolis (pharmacology), Reactive Oxygen Species (metabolism), Signal Transduction (drug effects), Transcription Factor RelA (metabolism), Tumor Suppressor Protein p53 (metabolism), p38 Mitogen-Activated Protein Kinases (metabolism).
MESH :
- chemical , metabolism : NF-kappa B, Reactive Oxygen Species, Transcription Factor RelA, Tumor Suppressor Protein p53, p38 Mitogen-Activated Protein Kinases.
- chemical , pharmacology : Anti-Inflammatory Agents, Lipopolysaccharides, Propolis.
- drug effects : Autophagy, Cell Proliferation, Human Umbilical Vein Endothelial Cells, MAP Kinase Signaling System, Membrane Potential, Mitochondrial, Signal Transduction.
- drug therapy : Inflammation.
- metabolism : Human Umbilical Vein Endothelial Cells, Inflammation.
- Cell Line, Humans.

Abstract

This study aimed to investigate the possible benefits of Chinese poplar propolis (CP) in inhibiting inflammation using vascular endothelial cells (VECs) cultured in a nutrient-rich condition exposed to lipopolysaccharide (LPS). Cell proliferation was detected by sulforhodamine B assay and EdU kit. The production of reactive oxygen species (ROS) and level of mitochondrial membrane potential were determined with fluorescent probe DCHF and JC-1, respectively. Protein expression was examined by immunofluorescence staining and western blotting. The results showed that CP (6.25, 12.5, and 25 μg/mL) significantly reduced LPS-induced cytotoxicity, and when challenged with CP substantially suppressed ROS overproduction and protected mitochondrial membrane potential. CP treatment significantly inhibited autophagy by inhibiting LC3B distribution and accumulation, and elevating the p62 level in an mTOR-independent manner but mainly by suppressing the translocation of p53 from the cytoplasm to the nucleus. Furthermore, CP treatment markedly reduced protein levels of TLR4 at 12 and 24 h and significantly suppressed nuclear translocation of NF-κB p65 from cytoplasm to nucleus. In addition, CP treatment significantly reduced the phosphorylation of JNK, ERK1/2, and p38 MAPK. Our findings demonstrated that CP protects VECs from LPS-induced oxidative stress and inflammation, which might be associated with depressing autophagy and MAPK/NF-κB signaling pathway. The results provided novel insights for the potential use of nutrient-rich propolis against inflammation.

DOI: 10.1007/s10787-018-0533-6
PubMed: 30251233

Affiliations:

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

to stream Main, to step Corpus: 000C52
to stream Main, to step Curation: 000C52

Le document en format XML

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<term>Autophagy (drug effects)</term>
<term>Cell Line (MeSH)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Human Umbilical Vein Endothelial Cells (drug effects)</term>
<term>Human Umbilical Vein Endothelial Cells (metabolism)</term>
<term>Humans (MeSH)</term>
<term>Inflammation (drug therapy)</term>
<term>Inflammation (metabolism)</term>
<term>Lipopolysaccharides (pharmacology)</term>
<term>MAP Kinase Signaling System (drug effects)</term>
<term>Membrane Potential, Mitochondrial (drug effects)</term>
<term>NF-kappa B (metabolism)</term>
<term>Propolis (pharmacology)</term>
<term>Reactive Oxygen Species (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Transcription Factor RelA (metabolism)</term>
<term>Tumor Suppressor Protein p53 (metabolism)</term>
<term>p38 Mitogen-Activated Protein Kinases (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Anti-inflammatoires (pharmacologie)</term>
<term>Autophagie (effets des médicaments et des substances chimiques)</term>
<term>Cellules endothéliales de la veine ombilicale humaine (effets des médicaments et des substances chimiques)</term>
<term>Cellules endothéliales de la veine ombilicale humaine (métabolisme)</term>
<term>Espèces réactives de l'oxygène (métabolisme)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Facteur de transcription RelA (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Inflammation (métabolisme)</term>
<term>Inflammation (traitement médicamenteux)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lipopolysaccharides (pharmacologie)</term>
<term>Potentiel de membrane mitochondriale (effets des médicaments et des substances chimiques)</term>
<term>Prolifération cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Propolis (pharmacologie)</term>
<term>Protéine p53 suppresseur de tumeur (métabolisme)</term>
<term>Système de signalisation des MAP kinases (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>p38 Mitogen-Activated Protein Kinases (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>NF-kappa B</term>
<term>Reactive Oxygen Species</term>
<term>Transcription Factor RelA</term>
<term>Tumor Suppressor Protein p53</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term>
<term>Lipopolysaccharides</term>
<term>Propolis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Cell Proliferation</term>
<term>Human Umbilical Vein Endothelial Cells</term>
<term>MAP Kinase Signaling System</term>
<term>Membrane Potential, Mitochondrial</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Inflammation</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Autophagie</term>
<term>Cellules endothéliales de la veine ombilicale humaine</term>
<term>Potentiel de membrane mitochondriale</term>
<term>Prolifération cellulaire</term>
<term>Système de signalisation des MAP kinases</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Human Umbilical Vein Endothelial Cells</term>
<term>Inflammation</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales de la veine ombilicale humaine</term>
<term>Espèces réactives de l'oxygène</term>
<term>Facteur de transcription NF-kappa B</term>
<term>Facteur de transcription RelA</term>
<term>Inflammation</term>
<term>Protéine p53 suppresseur de tumeur</term>
<term>p38 Mitogen-Activated Protein Kinases</term>
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<term>Lipopolysaccharides</term>
<term>Propolis</term>
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</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Humains</term>
<term>Lignée cellulaire</term>
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<front><div type="abstract" xml:lang="en">This study aimed to investigate the possible benefits of Chinese poplar propolis (CP) in inhibiting inflammation using vascular endothelial cells (VECs) cultured in a nutrient-rich condition exposed to lipopolysaccharide (LPS). Cell proliferation was detected by sulforhodamine B assay and EdU kit. The production of reactive oxygen species (ROS) and level of mitochondrial membrane potential were determined with fluorescent probe DCHF and JC-1, respectively. Protein expression was examined by immunofluorescence staining and western blotting. The results showed that CP (6.25, 12.5, and 25 μg/mL) significantly reduced LPS-induced cytotoxicity, and when challenged with CP substantially suppressed ROS overproduction and protected mitochondrial membrane potential. CP treatment significantly inhibited autophagy by inhibiting LC3B distribution and accumulation, and elevating the p62 level in an mTOR-independent manner but mainly by suppressing the translocation of p53 from the cytoplasm to the nucleus. Furthermore, CP treatment markedly reduced protein levels of TLR4 at 12 and 24 h and significantly suppressed nuclear translocation of NF-κB p65 from cytoplasm to nucleus. In addition, CP treatment significantly reduced the phosphorylation of JNK, ERK1/2, and p38 MAPK. Our findings demonstrated that CP protects VECs from LPS-induced oxidative stress and inflammation, which might be associated with depressing autophagy and MAPK/NF-κB signaling pathway. The results provided novel insights for the potential use of nutrient-rich propolis against inflammation.</div>
</front>
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<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30251233</PMID>
<DateCompleted><Year>2019</Year>
<Month>11</Month>
<Day>27</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>02</Month>
<Day>25</Day>
</DateRevised>
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<JournalIssue CitedMedium="Internet"><Volume>27</Volume>
<Issue>3</Issue>
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<Month>Jun</Month>
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<Title>Inflammopharmacology</Title>
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<ArticleTitle>Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.</ArticleTitle>
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<Abstract><AbstractText>This study aimed to investigate the possible benefits of Chinese poplar propolis (CP) in inhibiting inflammation using vascular endothelial cells (VECs) cultured in a nutrient-rich condition exposed to lipopolysaccharide (LPS). Cell proliferation was detected by sulforhodamine B assay and EdU kit. The production of reactive oxygen species (ROS) and level of mitochondrial membrane potential were determined with fluorescent probe DCHF and JC-1, respectively. Protein expression was examined by immunofluorescence staining and western blotting. The results showed that CP (6.25, 12.5, and 25 μg/mL) significantly reduced LPS-induced cytotoxicity, and when challenged with CP substantially suppressed ROS overproduction and protected mitochondrial membrane potential. CP treatment significantly inhibited autophagy by inhibiting LC3B distribution and accumulation, and elevating the p62 level in an mTOR-independent manner but mainly by suppressing the translocation of p53 from the cytoplasm to the nucleus. Furthermore, CP treatment markedly reduced protein levels of TLR4 at 12 and 24 h and significantly suppressed nuclear translocation of NF-κB p65 from cytoplasm to nucleus. In addition, CP treatment significantly reduced the phosphorylation of JNK, ERK1/2, and p38 MAPK. Our findings demonstrated that CP protects VECs from LPS-induced oxidative stress and inflammation, which might be associated with depressing autophagy and MAPK/NF-κB signaling pathway. The results provided novel insights for the potential use of nutrient-rich propolis against inflammation.</AbstractText>
</Abstract>
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<ForeName>Fuliang</ForeName>
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<AffiliationInfo><Affiliation>College of Animal Sciences, Zhejiang University, Hangzhou, 310029, China. flhu@zju.edu.cn.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Country></Country>
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<Country></Country>
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<MedlineTA>Inflammopharmacology</MedlineTA>
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<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
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<MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName>
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<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
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<MeshHeading><DescriptorName UI="D051996" MajorTopicYN="N">Transcription Factor RelA</DescriptorName>
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</MeshHeading>
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Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.

Anti-inflammatory effects of Chinese propolis in lipopolysaccharide-stimulated human umbilical vein endothelial cells by suppressing autophagy and MAPK/NF-κB signaling pathway.

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