Vascular protection of salicin on IL-1β-induced endothelial inflammatory response and damages in retinal endothelial cells.
Identifieur interne : 000452 ( Main/Corpus ); précédent : 000451; suivant : 000453Vascular protection of salicin on IL-1β-induced endothelial inflammatory response and damages in retinal endothelial cells.
Auteurs : Yu Song ; Xia Tian ; Xuehong Wang ; Hui FengSource :
- Artificial cells, nanomedicine, and biotechnology [ 2169-141X ] ; 2019.
English descriptors
- KwdEn :
- Benzyl Alcohols (pharmacology), Blood Vessels (cytology), Blood Vessels (drug effects), Cell Line (MeSH), Endothelial Cells (cytology), Endothelial Cells (drug effects), Endothelial Cells (metabolism), Gene Expression Regulation (drug effects), Glucosides (pharmacology), HMGB1 Protein (biosynthesis), Humans (MeSH), Inflammation (chemically induced), Inflammation (pathology), Intercellular Adhesion Molecule-1 (metabolism), Interleukin-1beta (pharmacology), Intracellular Space (drug effects), Intracellular Space (metabolism), L-Lactate Dehydrogenase (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), NF-kappa B (metabolism), Nitric Oxide (metabolism), Nitric Oxide Synthase Type III (metabolism), Oxidative Stress (drug effects), Reactive Oxygen Species (metabolism), Retina (cytology), Vascular Cell Adhesion Molecule-1 (metabolism).
- MESH :
- chemical , biosynthesis : HMGB1 Protein.
- chemical , metabolism : Intercellular Adhesion Molecule-1, L-Lactate Dehydrogenase, NF-kappa B, Nitric Oxide, Nitric Oxide Synthase Type III, Reactive Oxygen Species, Vascular Cell Adhesion Molecule-1.
- chemical , pharmacology : Benzyl Alcohols, Glucosides, Interleukin-1beta.
- chemically induced : Inflammation.
- cytology : Blood Vessels, Endothelial Cells, Retina.
- drug effects : Blood Vessels, Endothelial Cells, Gene Expression Regulation, Intracellular Space, Mitochondria, Oxidative Stress.
- metabolism : Endothelial Cells, Intracellular Space, Mitochondria.
- pathology : Inflammation.
- Cell Line, Humans.
Abstract
Retinal endothelial cells (RECs) are involved in many ocular diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Salicin is the major ingredient of willow bark extract, and it has been shown to be a potent anti-inflammatory agent. We aim to explore whether salicin has a vascular protective effect in RECs. Our data indicate that the presence of salicin in RECs culture media ameliorates interleukin-1β (IL-1β)-induced cellular reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX-4) expression. At the cellular level, salicin attenuates IL-1β-induced mitochondrial injury as revealed by its preservation on mitochondrial membrane potential (MMP). Furthermore, salicin inhibits IL-1β-induced production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1). On the other hand, salicin recovers IL-1β-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release. The presence of salicin significantly reduces the IL-1β-induced release of lactate dehydrogenase (LDH), indicating that it mitigates cytokine caused cytotoxicity. Mechanistically, we show that salicin suppresses IL-1β-induced activation of the nuclear factor-kappa B (NF-κB) signaling as revealed by its suppression on nuclear p65 protein and transfected NF-κB promoter. Collectively, our study demonstrates by multiple facets of its mechanisms that salicin is a protective agent in retinal endothelial cells. These results imply its potential use in therapeutic usage of retinal disease.
DOI: 10.1080/21691401.2019.1608220
PubMed: 31106593
Links to Exploration step
pubmed:31106593Le document en format XML
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sort="Feng, Hui" uniqKey="Feng H" first="Hui" last="Feng">Hui Feng</name><affiliation><nlm:affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2019">2019</date><idno type="RBID">pubmed:31106593</idno><idno type="pmid">31106593</idno><idno type="doi">10.1080/21691401.2019.1608220</idno><idno type="wicri:Area/Main/Corpus">000452</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">000452</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Vascular protection of salicin on IL-1β-induced endothelial inflammatory response and damages in retinal endothelial cells.</title><author><name sortKey="Song, Yu" sort="Song, Yu" uniqKey="Song Y" first="Yu" last="Song">Yu Song</name><affiliation><nlm:affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</nlm:affiliation></affiliation></author><author><name sortKey="Tian, Xia" sort="Tian, Xia" uniqKey="Tian X" first="Xia" last="Tian">Xia Tian</name><affiliation><nlm:affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Xuehong" sort="Wang, Xuehong" uniqKey="Wang X" first="Xuehong" last="Wang">Xuehong Wang</name><affiliation><nlm:affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</nlm:affiliation></affiliation></author><author><name sortKey="Feng, Hui" sort="Feng, Hui" uniqKey="Feng H" first="Hui" last="Feng">Hui Feng</name><affiliation><nlm:affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Artificial cells, nanomedicine, and biotechnology</title><idno type="eISSN">2169-141X</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Benzyl Alcohols (pharmacology)</term><term>Blood Vessels (cytology)</term><term>Blood Vessels (drug effects)</term><term>Cell Line (MeSH)</term><term>Endothelial Cells (cytology)</term><term>Endothelial Cells (drug effects)</term><term>Endothelial Cells (metabolism)</term><term>Gene Expression Regulation (drug effects)</term><term>Glucosides (pharmacology)</term><term>HMGB1 Protein (biosynthesis)</term><term>Humans (MeSH)</term><term>Inflammation (chemically induced)</term><term>Inflammation (pathology)</term><term>Intercellular Adhesion Molecule-1 (metabolism)</term><term>Interleukin-1beta (pharmacology)</term><term>Intracellular Space (drug effects)</term><term>Intracellular Space (metabolism)</term><term>L-Lactate Dehydrogenase (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>NF-kappa B (metabolism)</term><term>Nitric Oxide (metabolism)</term><term>Nitric Oxide Synthase Type III (metabolism)</term><term>Oxidative Stress (drug effects)</term><term>Reactive Oxygen Species (metabolism)</term><term>Retina (cytology)</term><term>Vascular Cell Adhesion Molecule-1 (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>HMGB1 Protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Intercellular Adhesion Molecule-1</term><term>L-Lactate Dehydrogenase</term><term>NF-kappa B</term><term>Nitric Oxide</term><term>Nitric Oxide Synthase Type III</term><term>Reactive Oxygen Species</term><term>Vascular Cell Adhesion Molecule-1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Benzyl Alcohols</term><term>Glucosides</term><term>Interleukin-1beta</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Blood Vessels</term><term>Endothelial Cells</term><term>Retina</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Blood Vessels</term><term>Endothelial Cells</term><term>Gene Expression Regulation</term><term>Intracellular Space</term><term>Mitochondria</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term><term>Intracellular Space</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Line</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Retinal endothelial cells (RECs) are involved in many ocular diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Salicin is the major ingredient of willow bark extract, and it has been shown to be a potent anti-inflammatory agent. We aim to explore whether salicin has a vascular protective effect in RECs. Our data indicate that the presence of salicin in RECs culture media ameliorates interleukin-1β (IL-1β)-induced cellular reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX-4) expression. At the cellular level, salicin attenuates IL-1β-induced mitochondrial injury as revealed by its preservation on mitochondrial membrane potential (MMP). Furthermore, salicin inhibits IL-1β-induced production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1). On the other hand, salicin recovers IL-1β-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release. The presence of salicin significantly reduces the IL-1β-induced release of lactate dehydrogenase (LDH), indicating that it mitigates cytokine caused cytotoxicity. Mechanistically, we show that salicin suppresses IL-1β-induced activation of the nuclear factor-kappa B (NF-κB) signaling as revealed by its suppression on nuclear p65 protein and transfected NF-κB promoter. Collectively, our study demonstrates by multiple facets of its mechanisms that salicin is a protective agent in retinal endothelial cells. These results imply its potential use in therapeutic usage of retinal disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31106593</PMID><DateCompleted><Year>2019</Year><Month>11</Month><Day>04</Day></DateCompleted><DateRevised><Year>2019</Year><Month>11</Month><Day>04</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">2169-141X</ISSN><JournalIssue CitedMedium="Internet"><Volume>47</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Artificial cells, nanomedicine, and biotechnology</Title><ISOAbbreviation>Artif Cells Nanomed Biotechnol</ISOAbbreviation></Journal><ArticleTitle>Vascular protection of salicin on IL-1β-induced endothelial inflammatory response and damages in retinal endothelial cells.</ArticleTitle><Pagination><MedlinePgn>1995-2002</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1080/21691401.2019.1608220</ELocationID><Abstract><AbstractText>Retinal endothelial cells (RECs) are involved in many ocular diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Salicin is the major ingredient of willow bark extract, and it has been shown to be a potent anti-inflammatory agent. We aim to explore whether salicin has a vascular protective effect in RECs. Our data indicate that the presence of salicin in RECs culture media ameliorates interleukin-1β (IL-1β)-induced cellular reactive oxygen species (ROS) production and NADPH oxidase 4 (NOX-4) expression. At the cellular level, salicin attenuates IL-1β-induced mitochondrial injury as revealed by its preservation on mitochondrial membrane potential (MMP). Furthermore, salicin inhibits IL-1β-induced production of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1), vascular adhesion molecules such as intercellular cell adhesion molecule-1 (iCAM-1) and vascular cell adhesion molecule 1 (VCAM-1), and high-mobility group protein 1 (HMGB-1). On the other hand, salicin recovers IL-1β-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release. The presence of salicin significantly reduces the IL-1β-induced release of lactate dehydrogenase (LDH), indicating that it mitigates cytokine caused cytotoxicity. Mechanistically, we show that salicin suppresses IL-1β-induced activation of the nuclear factor-kappa B (NF-κB) signaling as revealed by its suppression on nuclear p65 protein and transfected NF-κB promoter. Collectively, our study demonstrates by multiple facets of its mechanisms that salicin is a protective agent in retinal endothelial cells. These results imply its potential use in therapeutic usage of retinal disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Song</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tian</LastName><ForeName>Xia</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xuehong</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feng</LastName><ForeName>Hui</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>a Department of ophthalmology, Weihai Central hospital , Weihai , China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Artif Cells Nanomed Biotechnol</MedlineTA><NlmUniqueID>101594777</NlmUniqueID><ISSNLinking>2169-1401</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D001592">Benzyl Alcohols</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005960">Glucosides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024243">HMGB1 Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053583">Interleukin-1beta</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016328">NF-kappa B</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</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></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>4649620TBZ</RegistryNumber><NameOfSubstance UI="C005696">salicin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.1.1.27</RegistryNumber><NameOfSubstance UI="D007770">L-Lactate Dehydrogenase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber><NameOfSubstance UI="D052250">Nitric Oxide Synthase Type III</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001592" MajorTopicYN="N">Benzyl Alcohols</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001808" MajorTopicYN="N">Blood Vessels</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005960" MajorTopicYN="N">Glucosides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D024243" MajorTopicYN="N">HMGB1 Protein</DescriptorName><QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018799" MajorTopicYN="N">Intercellular Adhesion Molecule-1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053583" MajorTopicYN="N">Interleukin-1beta</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042541" MajorTopicYN="N">Intracellular Space</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007770" MajorTopicYN="N">L-Lactate Dehydrogenase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016328" MajorTopicYN="N">NF-kappa B</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052250" MajorTopicYN="N">Nitric Oxide Synthase Type III</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012160" MajorTopicYN="N">Retina</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</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">IL-1β</Keyword><Keyword MajorTopicYN="N">NF-κB</Keyword><Keyword MajorTopicYN="N">Retinal endothelial cell (RECs)</Keyword><Keyword MajorTopicYN="N">inflammation</Keyword><Keyword MajorTopicYN="N">reactive oxygen species (ROS)</Keyword><Keyword MajorTopicYN="N">salicin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>5</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>5</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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