ChloroquineV1, PubMed, Curation, bibRecord, 000092

Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.

Identifieur interne : 000092 ( PubMed/Curation ); précédent : 000091; suivant : 000093

Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.

Source :

International immunopharmacology [ 1878-1705 ] ; 2018.

RBID : pubmed:30121047

Descripteurs français

English descriptors

KwdEn :
- Anti-Inflammatory Agents (pharmacology), Antimalarials (pharmacology), Cell Adhesion (drug effects), Cells, Cultured, Human Umbilical Vein Endothelial Cells (drug effects), Human Umbilical Vein Endothelial Cells (metabolism), Humans, Hydroxychloroquine (pharmacology), Intercellular Adhesion Molecule-1 (metabolism), Leukocytes (drug effects), Leukocytes (metabolism), MAP Kinase Signaling System (drug effects), Tumor Necrosis Factor-alpha (pharmacology), Vascular Cell Adhesion Molecule-1 (metabolism).
MESH :
- chemical , metabolism : Intercellular Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1.
- chemical , pharmacology : Anti-Inflammatory Agents, Antimalarials, Hydroxychloroquine, Tumor Necrosis Factor-alpha.
- drug effects : Cell Adhesion, Human Umbilical Vein Endothelial Cells, Leukocytes, MAP Kinase Signaling System.
- metabolism : Human Umbilical Vein Endothelial Cells, Leukocytes.
- Cells, Cultured, Humans.

Abstract

Hydroxychloroquine (HCQ) is an antimalarial drug that is widely used in the treatment of some autoimmune diseases. In the present study, we explore the role of HCQ in regulating endothelial inflammation and its underlying mechanism.

DOI: 10.1016/j.intimp.2018.08.008
PubMed: 30121047

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Le document en format XML

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<author><name sortKey="Lin, Haobo" sort="Lin, Haobo" uniqKey="Lin H" first="Haobo" last="Lin">Haobo Lin</name>
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<term>Cell Adhesion (drug effects)</term>
<term>Cells, Cultured</term>
<term>Human Umbilical Vein Endothelial Cells (drug effects)</term>
<term>Human Umbilical Vein Endothelial Cells (metabolism)</term>
<term>Humans</term>
<term>Hydroxychloroquine (pharmacology)</term>
<term>Intercellular Adhesion Molecule-1 (metabolism)</term>
<term>Leukocytes (drug effects)</term>
<term>Leukocytes (metabolism)</term>
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<term>Anti-inflammatoires (pharmacologie)</term>
<term>Antipaludiques (pharmacologie)</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales de la veine ombilicale humaine ()</term>
<term>Cellules endothéliales de la veine ombilicale humaine (métabolisme)</term>
<term>Facteur de nécrose tumorale alpha (pharmacologie)</term>
<term>Humains</term>
<term>Hydroxychloroquine (pharmacologie)</term>
<term>Leucocytes ()</term>
<term>Leucocytes (métabolisme)</term>
<term>Molécule-1 d'adhérence des cellules vasculaires (métabolisme)</term>
<term>Molécule-1 d'adhérence intercellulaire (métabolisme)</term>
<term>Système de signalisation des MAP kinases ()</term>
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<term>Vascular Cell Adhesion Molecule-1</term>
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<term>Antimalarials</term>
<term>Hydroxychloroquine</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Adhesion</term>
<term>Human Umbilical Vein Endothelial Cells</term>
<term>Leukocytes</term>
<term>MAP Kinase Signaling System</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Human Umbilical Vein Endothelial Cells</term>
<term>Leukocytes</term>
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<term>Leucocytes</term>
<term>Molécule-1 d'adhérence des cellules vasculaires</term>
<term>Molécule-1 d'adhérence intercellulaire</term>
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<term>Hydroxychloroquine</term>
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<term>Humans</term>
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<term>Cellules cultivées</term>
<term>Cellules endothéliales de la veine ombilicale humaine</term>
<term>Humains</term>
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<front><div type="abstract" xml:lang="en">Hydroxychloroquine (HCQ) is an antimalarial drug that is widely used in the treatment of some autoimmune diseases. In the present study, we explore the role of HCQ in regulating endothelial inflammation and its underlying mechanism.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30121047</PMID>
<DateCompleted><Year>2018</Year>
<Month>12</Month>
<Day>11</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>12</Month>
<Day>11</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-1705</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>63</Volume>
<PubDate><Year>2018</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>International immunopharmacology</Title>
<ISOAbbreviation>Int. Immunopharmacol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.</ArticleTitle>
<Pagination><MedlinePgn>261-269</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S1567-5769(18)30385-0</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.intimp.2018.08.008</ELocationID>
<Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Hydroxychloroquine (HCQ) is an antimalarial drug that is widely used in the treatment of some autoimmune diseases. In the present study, we explore the role of HCQ in regulating endothelial inflammation and its underlying mechanism.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Human umbilical vein endothelial cells (HUVECs) were isolated from fresh umbilical cords. Protein expression was measured by Western blot or immunofluorescence staining. Endothelial adhesion ability was determined by leukocyte-endothelial monolayer adhesion assay. Transwell assay was used to measure the transendothelial-migration of PBMCs.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">TNF-α-induced endothelial-leukocyte adhesion and the leukocyte transmigration were profoundly reduced by HCQ treatment. HCQ treatment dramatically inhibited the expression of TNF-α-induced endothelial ICAM-1 and VCAM-1. Furthermore, treatment with HCQ prevented the TNF-α-induced translocation of NF-κB p65 into the nucleus and the phosphorylation of the p65 subunit in HUVECs. HCQ inhibited the expression of phosphorylated p38 and JNK protein but not ERK. Treatment with NF-κB, p38 and JNK inhibitor could also reduce TNF-α-induced endothelial-leukocyte adhesion and the endothelial expression of ICAM-1 and VCAM-1. HCQ administration also suppressed TNF-α induced lung injury in mice by reducing neutrophil infiltration in pulmonary interstitial tissue.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">This work shows the inhibitory effect of HCQ on endothelial inflammatory response through, at least in part, blocking NF-κB, p38 and JNK pathways. Our findings suggest that HCQ may be a promising approach for the treatment of inflammatory vascular disease beyond its immunomodulatory actions.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Ruiru</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Haobo</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatism, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ye</LastName>
<ForeName>Yujin</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xiao</LastName>
<ForeName>Youjun</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Siqi</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Jingnan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Cuicui</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zou</LastName>
<ForeName>Yaoyao</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Shi</LastName>
<ForeName>Maohua</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liang</LastName>
<ForeName>Liuqin</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Hanshi</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong, PR China. Electronic address: xuhanshi@mail.sysu.edu.cn.</Affiliation>
</AffiliationInfo>
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<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>08</Month>
<Day>16</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Netherlands</Country>
<MedlineTA>Int Immunopharmacol</MedlineTA>
<NlmUniqueID>100965259</NlmUniqueID>
<ISSNLinking>1567-5769</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000962">Antimalarials</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019010">Vascular Cell Adhesion Molecule-1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>126547-89-5</RegistryNumber>
<NameOfSubstance UI="D018799">Intercellular Adhesion Molecule-1</NameOfSubstance>
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<Chemical><RegistryNumber>4QWG6N8QKH</RegistryNumber>
<NameOfSubstance UI="D006886">Hydroxychloroquine</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000962" MajorTopicYN="N">Antimalarials</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D002448" MajorTopicYN="N">Cell Adhesion</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D061307" MajorTopicYN="N">Human Umbilical Vein Endothelial Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006886" MajorTopicYN="N">Hydroxychloroquine</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
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<MeshHeading><DescriptorName UI="D018799" MajorTopicYN="N">Intercellular Adhesion Molecule-1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007962" MajorTopicYN="N">Leukocytes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020935" MajorTopicYN="N">MAP Kinase Signaling System</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019010" MajorTopicYN="N">Vascular Cell Adhesion Molecule-1</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Endothelial cells</Keyword>
<Keyword MajorTopicYN="N">Hydroxychloroquine</Keyword>
<Keyword MajorTopicYN="N">Inflammation</Keyword>
<Keyword MajorTopicYN="N">MAPK</Keyword>
<Keyword MajorTopicYN="N">NF-κB</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>04</Month>
<Day>28</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>08</Month>
<Day>01</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>08</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>8</Month>
<Day>19</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="medline"><Year>2018</Year>
<Month>12</Month>
<Day>12</Day>
<Hour>6</Hour>
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<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>8</Month>
<Day>19</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">30121047</ArticleId>
<ArticleId IdType="pii">S1567-5769(18)30385-0</ArticleId>
<ArticleId IdType="doi">10.1016/j.intimp.2018.08.008</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>

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   |texte=   Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.
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Serveur d'exploration Chloroquine

Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.

Attenuation of antimalarial agent hydroxychloroquine on TNF-α-induced endothelial inflammation.

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