IMM-H004 protects against oxygen-glucose deprivation/reperfusion injury to BV2 microglia partly by modulating CKLF1 involved in microglia polarization
IMM-H004 is a novel compound that has been shown to protect against cerebral ischemia/reperfusion injury in our previous works. Chemokine-like factor 1 (CKLF1) is a chemokine that exhibits increased expression in the ischemic brain. Dysregulation of microglia polarization dynamics is a mechanism of...
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| Veröffentlicht in: | International immunopharmacology 2019-05, Vol.70, p.69-79 |
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| creator | Chen, Chen Ai, Qidi Chu, Shifeng Zhang, Zhao Zhou, Xin Luo, Piao Liu, Yingjiao Chen, Naihong |
| description | IMM-H004 is a novel compound that has been shown to protect against cerebral ischemia/reperfusion injury in our previous works. Chemokine-like factor 1 (CKLF1) is a chemokine that exhibits increased expression in the ischemic brain. Dysregulation of microglia polarization dynamics is a mechanism of injury expansion poststroke.
The aim of present study was to investigate the effects of IMM-H004 on cell viability and microglia phenotypes in BV2 microglia suffering from oxygen-glucose deprivation/reperfusion and discussing the involvement of CKLF1 and possible mechanisms.
IMM-H004 protected BV2 microglia from oxygen-glucose deprivation/reperfusion-induced toxicity. We found that the expression of CKLF1 was increased in BV2 microglia with oxygen-glucose deprivation/reperfusion, and IMM-H004 decreased this specially increased expression. Moreover, oxygen-glucose deprivation/reperfusion induced the BV2 microglia to polarize toward an M1 phenotype, and IMM-H004 modulated the polarization shift from the M1 phenotype and skewed toward the M2 phenotype, followed by suppressing the excessive inflammatory response and improving recovery. CKLF1 modulated BV2 microglia toward M1 polarization and induced an inflammatory response. By using receptor inhibitors, we found that OGD/R induced microglia polarization partly through CC chemokine receptor 4. Furthermore, the Co-IP assay showed that IMM-H004 decreased the amount of CKLF1 binding to CC chemokine receptor 4 in the BV2 microglia oxygen-glucose deprivation/reperfusion model.
IMM-H004 protects BV2 microglia against oxygen-glucose deprivation/reperfusion injury partly by modulating microglia polarization and further regulating the inflammatory response. The CKLF1/CCR4 axis may be involved in the protective effects of IMM-H004 modulating microglia polarization.
•IMM-H004 protects BV2 microglia against OGD/R-induced toxicity.•IMM-H004 modulates microglia polarization and following inflammatory response in BV2 microglia injured by OGD/R.•IMM-H004 exerts protective effects by modulating microglia polarization that may involve the CKLF1/CCR4 axis. |
| doi_str_mv | 10.1016/j.intimp.2019.02.012 |
| format | Article |
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The aim of present study was to investigate the effects of IMM-H004 on cell viability and microglia phenotypes in BV2 microglia suffering from oxygen-glucose deprivation/reperfusion and discussing the involvement of CKLF1 and possible mechanisms.
IMM-H004 protected BV2 microglia from oxygen-glucose deprivation/reperfusion-induced toxicity. We found that the expression of CKLF1 was increased in BV2 microglia with oxygen-glucose deprivation/reperfusion, and IMM-H004 decreased this specially increased expression. Moreover, oxygen-glucose deprivation/reperfusion induced the BV2 microglia to polarize toward an M1 phenotype, and IMM-H004 modulated the polarization shift from the M1 phenotype and skewed toward the M2 phenotype, followed by suppressing the excessive inflammatory response and improving recovery. CKLF1 modulated BV2 microglia toward M1 polarization and induced an inflammatory response. By using receptor inhibitors, we found that OGD/R induced microglia polarization partly through CC chemokine receptor 4. Furthermore, the Co-IP assay showed that IMM-H004 decreased the amount of CKLF1 binding to CC chemokine receptor 4 in the BV2 microglia oxygen-glucose deprivation/reperfusion model.
IMM-H004 protects BV2 microglia against oxygen-glucose deprivation/reperfusion injury partly by modulating microglia polarization and further regulating the inflammatory response. The CKLF1/CCR4 axis may be involved in the protective effects of IMM-H004 modulating microglia polarization.
•IMM-H004 protects BV2 microglia against OGD/R-induced toxicity.•IMM-H004 modulates microglia polarization and following inflammatory response in BV2 microglia injured by OGD/R.•IMM-H004 exerts protective effects by modulating microglia polarization that may involve the CKLF1/CCR4 axis.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/j.intimp.2019.02.012</identifier><identifier>PMID: 30785093</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Brain ; BV2 microglia ; Cell Differentiation ; Cell Line ; Cell Survival - drug effects ; Cell viability ; Chemokines ; Chemokines - metabolism ; CKLF1 ; Coumarins - pharmacology ; Cytokines - metabolism ; Deprivation ; Genotype & phenotype ; Glucose ; Glucose - metabolism ; IMM-H004 ; Inflammation ; Inflammatory response ; Injuries ; Ischemia ; MARVEL Domain-Containing Proteins - metabolism ; Microglia ; Microglia - drug effects ; Microglia - pathology ; Microglia polarization ; Neuroprotective Agents - pharmacology ; Occupational health ; OGD/R ; Oxygen ; Oxygen - metabolism ; Phenotypes ; Polarization ; Rats ; Receptors, CCR4 - metabolism ; Reperfusion ; Reperfusion Injury - drug therapy ; Th1 Cells - immunology ; Toxicity</subject><ispartof>International immunopharmacology, 2019-05, Vol.70, p.69-79</ispartof><rights>2019</rights><rights>Copyright © 2019. Published by Elsevier B.V.</rights><rights>Copyright Elsevier BV May 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-9258c4f897777a2281061de76b870205159cda7d7506603b619dd02dc5be1ab03</citedby><cites>FETCH-LOGICAL-c390t-9258c4f897777a2281061de76b870205159cda7d7506603b619dd02dc5be1ab03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.intimp.2019.02.012$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30785093$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Ai, Qidi</creatorcontrib><creatorcontrib>Chu, Shifeng</creatorcontrib><creatorcontrib>Zhang, Zhao</creatorcontrib><creatorcontrib>Zhou, Xin</creatorcontrib><creatorcontrib>Luo, Piao</creatorcontrib><creatorcontrib>Liu, Yingjiao</creatorcontrib><creatorcontrib>Chen, Naihong</creatorcontrib><title>IMM-H004 protects against oxygen-glucose deprivation/reperfusion injury to BV2 microglia partly by modulating CKLF1 involved in microglia polarization</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>IMM-H004 is a novel compound that has been shown to protect against cerebral ischemia/reperfusion injury in our previous works. Chemokine-like factor 1 (CKLF1) is a chemokine that exhibits increased expression in the ischemic brain. Dysregulation of microglia polarization dynamics is a mechanism of injury expansion poststroke.
The aim of present study was to investigate the effects of IMM-H004 on cell viability and microglia phenotypes in BV2 microglia suffering from oxygen-glucose deprivation/reperfusion and discussing the involvement of CKLF1 and possible mechanisms.
IMM-H004 protected BV2 microglia from oxygen-glucose deprivation/reperfusion-induced toxicity. We found that the expression of CKLF1 was increased in BV2 microglia with oxygen-glucose deprivation/reperfusion, and IMM-H004 decreased this specially increased expression. Moreover, oxygen-glucose deprivation/reperfusion induced the BV2 microglia to polarize toward an M1 phenotype, and IMM-H004 modulated the polarization shift from the M1 phenotype and skewed toward the M2 phenotype, followed by suppressing the excessive inflammatory response and improving recovery. CKLF1 modulated BV2 microglia toward M1 polarization and induced an inflammatory response. By using receptor inhibitors, we found that OGD/R induced microglia polarization partly through CC chemokine receptor 4. Furthermore, the Co-IP assay showed that IMM-H004 decreased the amount of CKLF1 binding to CC chemokine receptor 4 in the BV2 microglia oxygen-glucose deprivation/reperfusion model.
IMM-H004 protects BV2 microglia against oxygen-glucose deprivation/reperfusion injury partly by modulating microglia polarization and further regulating the inflammatory response. The CKLF1/CCR4 axis may be involved in the protective effects of IMM-H004 modulating microglia polarization.
•IMM-H004 protects BV2 microglia against OGD/R-induced toxicity.•IMM-H004 modulates microglia polarization and following inflammatory response in BV2 microglia injured by OGD/R.•IMM-H004 exerts protective effects by modulating microglia polarization that may involve the CKLF1/CCR4 axis.</description><subject>Animals</subject><subject>Brain</subject><subject>BV2 microglia</subject><subject>Cell Differentiation</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Chemokines</subject><subject>Chemokines - metabolism</subject><subject>CKLF1</subject><subject>Coumarins - pharmacology</subject><subject>Cytokines - metabolism</subject><subject>Deprivation</subject><subject>Genotype & phenotype</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>IMM-H004</subject><subject>Inflammation</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>MARVEL Domain-Containing Proteins - metabolism</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - pathology</subject><subject>Microglia polarization</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Occupational health</subject><subject>OGD/R</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Phenotypes</subject><subject>Polarization</subject><subject>Rats</subject><subject>Receptors, CCR4 - metabolism</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Th1 Cells - immunology</subject><subject>Toxicity</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1TAQhSMEoj_wBghZYtNN0rHz42SDBFeUVtyqG2BrOfbcyJETBzu5In0Qnre-3IIQi3rjI-ucGc98SfKGQkaBVpd9ZsbZDFPGgDYZsAwoe5ac0prXKeVQPo-6rHha8qo5Sc5C6AHie0FfJic58LqEJj9Nft3c3qbXAAWZvJtRzYHITpoxzMT9XDsc084uygUkGidv9nI2brz0OKHfLSFqYsZ-8SuZHfn4nZHBKO86aySZpJ_tStqVDE4vNgbHjmy-bK9ojOyd3aOO4t-As9Kb-98dXiUvdtIGfP14nyffrj593Vyn27vPN5sP21TlDcxpw8paFbu64fFIxmoKFdXIq7bmwKCkZaO05JqXUFWQtxVttAamVdkilS3k58nFsW6c_seCYRaDCQqtlSO6JQhG64IWDSsO1nf_WXu3-DH-TjBGK8YZ1Hl0FUdXnCoEjzsRtzZIvwoK4sBN9OLITRy4CWAicouxt4_Fl3ZA_Tf0B1Q0vD8aMG5jb9CLoAyOCrXxkZrQzjzd4QE7qawG</recordid><startdate>201905</startdate><enddate>201905</enddate><creator>Chen, Chen</creator><creator>Ai, Qidi</creator><creator>Chu, Shifeng</creator><creator>Zhang, Zhao</creator><creator>Zhou, Xin</creator><creator>Luo, Piao</creator><creator>Liu, Yingjiao</creator><creator>Chen, Naihong</creator><general>Elsevier B.V</general><general>Elsevier BV</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QO</scope><scope>7T5</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201905</creationdate><title>IMM-H004 protects against oxygen-glucose deprivation/reperfusion injury to BV2 microglia partly by modulating CKLF1 involved in microglia polarization</title><author>Chen, Chen ; Ai, Qidi ; Chu, Shifeng ; Zhang, Zhao ; Zhou, Xin ; Luo, Piao ; Liu, Yingjiao ; Chen, Naihong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-9258c4f897777a2281061de76b870205159cda7d7506603b619dd02dc5be1ab03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Brain</topic><topic>BV2 microglia</topic><topic>Cell Differentiation</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Cell viability</topic><topic>Chemokines</topic><topic>Chemokines - metabolism</topic><topic>CKLF1</topic><topic>Coumarins - pharmacology</topic><topic>Cytokines - metabolism</topic><topic>Deprivation</topic><topic>Genotype & phenotype</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>IMM-H004</topic><topic>Inflammation</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>MARVEL Domain-Containing Proteins - metabolism</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - pathology</topic><topic>Microglia polarization</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Occupational health</topic><topic>OGD/R</topic><topic>Oxygen</topic><topic>Oxygen - metabolism</topic><topic>Phenotypes</topic><topic>Polarization</topic><topic>Rats</topic><topic>Receptors, CCR4 - metabolism</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Th1 Cells - immunology</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chen</creatorcontrib><creatorcontrib>Ai, Qidi</creatorcontrib><creatorcontrib>Chu, Shifeng</creatorcontrib><creatorcontrib>Zhang, Zhao</creatorcontrib><creatorcontrib>Zhou, Xin</creatorcontrib><creatorcontrib>Luo, Piao</creatorcontrib><creatorcontrib>Liu, Yingjiao</creatorcontrib><creatorcontrib>Chen, Naihong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Immunology Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chen</au><au>Ai, Qidi</au><au>Chu, Shifeng</au><au>Zhang, Zhao</au><au>Zhou, Xin</au><au>Luo, Piao</au><au>Liu, Yingjiao</au><au>Chen, Naihong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>IMM-H004 protects against oxygen-glucose deprivation/reperfusion injury to BV2 microglia partly by modulating CKLF1 involved in microglia polarization</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2019-05</date><risdate>2019</risdate><volume>70</volume><spage>69</spage><epage>79</epage><pages>69-79</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>IMM-H004 is a novel compound that has been shown to protect against cerebral ischemia/reperfusion injury in our previous works. Chemokine-like factor 1 (CKLF1) is a chemokine that exhibits increased expression in the ischemic brain. Dysregulation of microglia polarization dynamics is a mechanism of injury expansion poststroke.
The aim of present study was to investigate the effects of IMM-H004 on cell viability and microglia phenotypes in BV2 microglia suffering from oxygen-glucose deprivation/reperfusion and discussing the involvement of CKLF1 and possible mechanisms.
IMM-H004 protected BV2 microglia from oxygen-glucose deprivation/reperfusion-induced toxicity. We found that the expression of CKLF1 was increased in BV2 microglia with oxygen-glucose deprivation/reperfusion, and IMM-H004 decreased this specially increased expression. Moreover, oxygen-glucose deprivation/reperfusion induced the BV2 microglia to polarize toward an M1 phenotype, and IMM-H004 modulated the polarization shift from the M1 phenotype and skewed toward the M2 phenotype, followed by suppressing the excessive inflammatory response and improving recovery. CKLF1 modulated BV2 microglia toward M1 polarization and induced an inflammatory response. By using receptor inhibitors, we found that OGD/R induced microglia polarization partly through CC chemokine receptor 4. Furthermore, the Co-IP assay showed that IMM-H004 decreased the amount of CKLF1 binding to CC chemokine receptor 4 in the BV2 microglia oxygen-glucose deprivation/reperfusion model.
IMM-H004 protects BV2 microglia against oxygen-glucose deprivation/reperfusion injury partly by modulating microglia polarization and further regulating the inflammatory response. The CKLF1/CCR4 axis may be involved in the protective effects of IMM-H004 modulating microglia polarization.
•IMM-H004 protects BV2 microglia against OGD/R-induced toxicity.•IMM-H004 modulates microglia polarization and following inflammatory response in BV2 microglia injured by OGD/R.•IMM-H004 exerts protective effects by modulating microglia polarization that may involve the CKLF1/CCR4 axis.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>30785093</pmid><doi>10.1016/j.intimp.2019.02.012</doi><tpages>11</tpages></addata></record> |
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| subjects | Animals Brain BV2 microglia Cell Differentiation Cell Line Cell Survival - drug effects Cell viability Chemokines Chemokines - metabolism CKLF1 Coumarins - pharmacology Cytokines - metabolism Deprivation Genotype & phenotype Glucose Glucose - metabolism IMM-H004 Inflammation Inflammatory response Injuries Ischemia MARVEL Domain-Containing Proteins - metabolism Microglia Microglia - drug effects Microglia - pathology Microglia polarization Neuroprotective Agents - pharmacology Occupational health OGD/R Oxygen Oxygen - metabolism Phenotypes Polarization Rats Receptors, CCR4 - metabolism Reperfusion Reperfusion Injury - drug therapy Th1 Cells - immunology Toxicity |
| title | IMM-H004 protects against oxygen-glucose deprivation/reperfusion injury to BV2 microglia partly by modulating CKLF1 involved in microglia polarization |
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