Salvianolate reduces neuronal apoptosis by suppressing OGD-induced microglial activation.
Identifieur interne : 000056 ( Main/Corpus ); précédent : 000055; suivant : 000057Salvianolate reduces neuronal apoptosis by suppressing OGD-induced microglial activation.
Auteurs : Pengwei Luan ; Xinyue Ding ; Jiazhen Xu ; Lixian Jiang ; Yulan Xu ; Yuying Zhu ; Ruixiang Li ; Jiange ZhangSource :
- Life sciences [ 1879-0631 ] ; 2020.
English descriptors
- KwdEn :
- Animals (MeSH), Apoptosis (MeSH), Cells, Cultured (MeSH), Cytokines (metabolism), Glucose (deficiency), Inflammation (drug therapy), Inflammation (metabolism), Inflammation (pathology), Mice (MeSH), Microglia (drug effects), Microglia (metabolism), Microglia (pathology), Neurons (drug effects), Neurons (metabolism), Neurons (pathology), Neuroprotective Agents (pharmacology), Oxygen (metabolism), Plant Extracts (pharmacology), Reactive Oxygen Species (metabolism), Signal Transduction (MeSH), Toll-Like Receptor 4 (metabolism).
- MESH :
- chemical , deficiency : Glucose.
- chemical , metabolism : Cytokines, Oxygen, Reactive Oxygen Species, Toll-Like Receptor 4.
- drug effects : Microglia, Neurons.
- drug therapy : Inflammation.
- metabolism : Inflammation, Microglia, Neurons.
- pathology : Inflammation, Microglia, Neurons.
- chemical , pharmacology : Neuroprotective Agents, Plant Extracts.
- Animals, Apoptosis, Cells, Cultured, Mice, Signal Transduction.
Abstract
AIMS
The aim of this study was to investigate the mechanism of pro-inflammatory phenotype transformation of microglia induced by oxygen-glucose deprivation (OGD), and how salvianolate regulates the polarization of microglia to exert neuroprotective effects.
MAIN METHODS
The immunofluorescence and western blot experiments were used to verify the injury effect on neuronal cells after inflammatory polarization of microglia. Secondly, immunofluorescence staining and western blot were analyzed inflammatory phenotype of microglia and TLR4 signaling pathway after salvianolate treatment. RT-qPCR and ELISA assays were showed the levels of RNA and proteins of inflammatory factors in microglia. Finally, flow cytometry and western blot assay proved that salvianolate had a certain protective effect on neuronal injury after inhibiting the phenotype of microglia.
KEY FINDINGS
The OGD condition could promote inflammation and activate of TLR4 signal pathway in microglia, and the polarization of microglia triggered caspase-3 signal pathway of neuronal cell. The optimal concentrations of salvianolate were incubated with microglia under OGD condition, which could reduce the reactive oxygen species (ROS) expression (P = 0.002) and also regulate the activity of SOD, CAT and GSH-px enzymes (P < 0.05). Moreover, salvianolate treatment could inhibit TLR4 signal pathway (P = 0.012), suppress the pro-inflammatory phenotype of microglia in OGD condition (P = 0.018), and reduce the expression of IL-6 and TNF-α (P < 0.05). Finally, neuronal damage induced by microglia under OGD condition was reversed after administration of the microglia supernatant after salvianolate treatment.
SIGNIFICANCE
Salvianolate, as an antioxidant, plays a neuroprotective role by inhibiting the pro-inflammatory phenotype and decreasing the expression of ROS in microglia.
DOI: 10.1016/j.lfs.2020.118393
PubMed: 32898527
Links to Exploration step
pubmed:32898527Le document en format XML
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Electronic address: jgzhang@shutcm.edu.cn.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2020">2020</date><idno type="RBID">pubmed:32898527</idno><idno type="pmid">32898527</idno><idno type="doi">10.1016/j.lfs.2020.118393</idno><idno type="wicri:Area/Main/Corpus">000056</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000056</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Salvianolate reduces neuronal apoptosis by suppressing OGD-induced microglial activation.</title><author><name sortKey="Luan, Pengwei" sort="Luan, Pengwei" uniqKey="Luan P" first="Pengwei" last="Luan">Pengwei Luan</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China.</nlm:affiliation></affiliation></author><author><name sortKey="Ding, Xinyue" sort="Ding, Xinyue" uniqKey="Ding X" first="Xinyue" last="Ding">Xinyue Ding</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xu, Jiazhen" sort="Xu, Jiazhen" uniqKey="Xu J" first="Jiazhen" last="Xu">Jiazhen Xu</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Jiang, Lixian" sort="Jiang, Lixian" uniqKey="Jiang L" first="Lixian" last="Jiang">Lixian Jiang</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Xu, Yulan" sort="Xu, Yulan" uniqKey="Xu Y" first="Yulan" last="Xu">Yulan Xu</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhu, Yuying" sort="Zhu, Yuying" uniqKey="Zhu Y" first="Yuying" last="Zhu">Yuying Zhu</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Li, Ruixiang" sort="Li, Ruixiang" uniqKey="Li R" first="Ruixiang" last="Li">Ruixiang Li</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</nlm:affiliation></affiliation></author><author><name sortKey="Zhang, Jiange" sort="Zhang, Jiange" uniqKey="Zhang J" first="Jiange" last="Zhang">Jiange Zhang</name><affiliation><nlm:affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address: jgzhang@shutcm.edu.cn.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Life sciences</title><idno type="eISSN">1879-0631</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Apoptosis (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Cytokines (metabolism)</term><term>Glucose (deficiency)</term><term>Inflammation (drug therapy)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Mice (MeSH)</term><term>Microglia (drug effects)</term><term>Microglia (metabolism)</term><term>Microglia (pathology)</term><term>Neurons (drug effects)</term><term>Neurons (metabolism)</term><term>Neurons (pathology)</term><term>Neuroprotective Agents (pharmacology)</term><term>Oxygen (metabolism)</term><term>Plant Extracts (pharmacology)</term><term>Reactive Oxygen Species (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Toll-Like Receptor 4 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glucose</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Oxygen</term><term>Reactive Oxygen Species</term><term>Toll-Like Receptor 4</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Microglia</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Microglia</term><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Microglia</term><term>Neurons</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term><term>Plant Extracts</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Cells, Cultured</term><term>Mice</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>The aim of this study was to investigate the mechanism of pro-inflammatory phenotype transformation of microglia induced by oxygen-glucose deprivation (OGD), and how salvianolate regulates the polarization of microglia to exert neuroprotective effects.</p></div><div type="abstract" xml:lang="en"><p><b>MAIN METHODS</b></p><p>The immunofluorescence and western blot experiments were used to verify the injury effect on neuronal cells after inflammatory polarization of microglia. Secondly, immunofluorescence staining and western blot were analyzed inflammatory phenotype of microglia and TLR4 signaling pathway after salvianolate treatment. RT-qPCR and ELISA assays were showed the levels of RNA and proteins of inflammatory factors in microglia. Finally, flow cytometry and western blot assay proved that salvianolate had a certain protective effect on neuronal injury after inhibiting the phenotype of microglia.</p></div><div type="abstract" xml:lang="en"><p><b>KEY FINDINGS</b></p><p>The OGD condition could promote inflammation and activate of TLR4 signal pathway in microglia, and the polarization of microglia triggered caspase-3 signal pathway of neuronal cell. The optimal concentrations of salvianolate were incubated with microglia under OGD condition, which could reduce the reactive oxygen species (ROS) expression (P = 0.002) and also regulate the activity of SOD, CAT and GSH-px enzymes (P < 0.05). Moreover, salvianolate treatment could inhibit TLR4 signal pathway (P = 0.012), suppress the pro-inflammatory phenotype of microglia in OGD condition (P = 0.018), and reduce the expression of IL-6 and TNF-α (P < 0.05). Finally, neuronal damage induced by microglia under OGD condition was reversed after administration of the microglia supernatant after salvianolate treatment.</p></div><div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b></p><p>Salvianolate, as an antioxidant, plays a neuroprotective role by inhibiting the pro-inflammatory phenotype and decreasing the expression of ROS in microglia.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32898527</PMID><DateCompleted><Year>2020</Year><Month>11</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0631</ISSN><JournalIssue CitedMedium="Internet"><Volume>260</Volume><PubDate><Year>2020</Year><Month>Nov</Month><Day>01</Day></PubDate></JournalIssue><Title>Life sciences</Title><ISOAbbreviation>Life Sci</ISOAbbreviation></Journal><ArticleTitle>Salvianolate reduces neuronal apoptosis by suppressing OGD-induced microglial activation.</ArticleTitle><Pagination><MedlinePgn>118393</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0024-3205(20)31146-2</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lfs.2020.118393</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">The aim of this study was to investigate the mechanism of pro-inflammatory phenotype transformation of microglia induced by oxygen-glucose deprivation (OGD), and how salvianolate regulates the polarization of microglia to exert neuroprotective effects.</AbstractText><AbstractText Label="MAIN METHODS" NlmCategory="METHODS">The immunofluorescence and western blot experiments were used to verify the injury effect on neuronal cells after inflammatory polarization of microglia. Secondly, immunofluorescence staining and western blot were analyzed inflammatory phenotype of microglia and TLR4 signaling pathway after salvianolate treatment. RT-qPCR and ELISA assays were showed the levels of RNA and proteins of inflammatory factors in microglia. Finally, flow cytometry and western blot assay proved that salvianolate had a certain protective effect on neuronal injury after inhibiting the phenotype of microglia.</AbstractText><AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">The OGD condition could promote inflammation and activate of TLR4 signal pathway in microglia, and the polarization of microglia triggered caspase-3 signal pathway of neuronal cell. The optimal concentrations of salvianolate were incubated with microglia under OGD condition, which could reduce the reactive oxygen species (ROS) expression (P = 0.002) and also regulate the activity of SOD, CAT and GSH-px enzymes (P < 0.05). Moreover, salvianolate treatment could inhibit TLR4 signal pathway (P = 0.012), suppress the pro-inflammatory phenotype of microglia in OGD condition (P = 0.018), and reduce the expression of IL-6 and TNF-α (P < 0.05). Finally, neuronal damage induced by microglia under OGD condition was reversed after administration of the microglia supernatant after salvianolate treatment.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Salvianolate, as an antioxidant, plays a neuroprotective role by inhibiting the pro-inflammatory phenotype and decreasing the expression of ROS in microglia.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Luan</LastName><ForeName>Pengwei</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ding</LastName><ForeName>Xinyue</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Jiazhen</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Lixian</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Yulan</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450001, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Yuying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Ruixiang</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Jiange</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>The Research Center of Chiral Drugs, Innovation Research Institute of Traditional, Chinese Medicine (IRI), Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address: jgzhang@shutcm.edu.cn.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>09</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018696">Neuroprotective Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010936">Plant Extracts</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051197">Toll-Like Receptor 4</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C561960">salvianolate</NameOfSubstance></Chemical><Chemical><RegistryNumber>IY9XDZ35W2</RegistryNumber><NameOfSubstance UI="D005947">Glucose</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005947" MajorTopicYN="N">Glucose</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017628" MajorTopicYN="N">Microglia</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018696" MajorTopicYN="N">Neuroprotective Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010936" MajorTopicYN="N">Plant Extracts</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051197" MajorTopicYN="N">Toll-Like Receptor 4</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Caspas-3 signal pathway</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Microglia</Keyword><Keyword MajorTopicYN="N">Neuronal apoptosis</Keyword><Keyword MajorTopicYN="N">ROS</Keyword><Keyword MajorTopicYN="N">TLR4 signal pathway</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>07</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>08</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>09</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>9</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>9</Month><Day>8</Day><Hour>20</Hour><Minute>7</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32898527</ArticleId><ArticleId IdType="pii">S0024-3205(20)31146-2</ArticleId><ArticleId IdType="doi">10.1016/j.lfs.2020.118393</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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