Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway
Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3'-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain...
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| Veröffentlicht in: | International journal of biological sciences 2021, Vol.17 (4), p.1088-1100 |
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| creator | Liu, Chaoming Liu, Song Xiong, Lijiao Zhang, Limei Li, Xiao Cao, Xingling Xue, Jinhua Li, Liangdong Huang, Cheng Huang, Zhihua |
| description | Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3'-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain injury in ischemic stroke by regulating microglial M1 depolarization and its underlying mechanisms. We established transient middle cerebral artery occlusion and reperfusion (tMCAO) model in rats and used lipopolysaccharide (LPS)-stimulated BV2 microglial cells as
model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1β level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke. |
| doi_str_mv | 10.7150/ijbs.56800 |
| format | Article |
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model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1β level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke.</description><identifier>ISSN: 1449-2288</identifier><identifier>EISSN: 1449-2288</identifier><identifier>DOI: 10.7150/ijbs.56800</identifier><identifier>PMID: 33867831</identifier><language>eng</language><publisher>Australia: Ivyspring International Publisher Pty Ltd</publisher><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Animals ; Blood-brain barrier ; Brain ; Brain Infarction - prevention & control ; Brain injury ; Cell Line ; Cerebral blood flow ; Cytokines ; Depolarization ; Drug Evaluation, Preclinical ; Estrogens ; Experiments ; Genistein ; Genistein - analogs & derivatives ; Genistein - pharmacology ; Genistein - therapeutic use ; Genotype & phenotype ; Head injuries ; IL-1β ; Inflammation ; Injury prevention ; Ischemia ; Ischemic Stroke - drug therapy ; Ischemic Stroke - metabolism ; Laboratories ; Lipopolysaccharides ; Male ; Mice ; Microglia ; Microglia - drug effects ; Microglial cells ; Neuroinflammatory Diseases - prevention & control ; Neuroprotection ; NF-kappa B - metabolism ; NF-κB protein ; Occlusion ; Penicillin ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Research Paper ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Sodium ; Stroke ; Sulfonates ; Traumatic brain injury ; Tumor necrosis factor-TNF ; Veins & arteries</subject><ispartof>International journal of biological sciences, 2021, Vol.17 (4), p.1088-1100</ispartof><rights>The author(s).</rights><rights>2021. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3210-bbde00fc936dcdcbb231a027d8a99b5a70098386eb804159fdd3a601ac47dc713</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040300/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8040300/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33867831$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Chaoming</creatorcontrib><creatorcontrib>Liu, Song</creatorcontrib><creatorcontrib>Xiong, Lijiao</creatorcontrib><creatorcontrib>Zhang, Limei</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Cao, Xingling</creatorcontrib><creatorcontrib>Xue, Jinhua</creatorcontrib><creatorcontrib>Li, Liangdong</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Huang, Zhihua</creatorcontrib><title>Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway</title><title>International journal of biological sciences</title><addtitle>Int J Biol Sci</addtitle><description>Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3'-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain injury in ischemic stroke by regulating microglial M1 depolarization and its underlying mechanisms. We established transient middle cerebral artery occlusion and reperfusion (tMCAO) model in rats and used lipopolysaccharide (LPS)-stimulated BV2 microglial cells as
model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1β level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke.</description><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Animals</subject><subject>Blood-brain barrier</subject><subject>Brain</subject><subject>Brain Infarction - prevention & control</subject><subject>Brain injury</subject><subject>Cell Line</subject><subject>Cerebral blood flow</subject><subject>Cytokines</subject><subject>Depolarization</subject><subject>Drug Evaluation, Preclinical</subject><subject>Estrogens</subject><subject>Experiments</subject><subject>Genistein</subject><subject>Genistein - analogs & derivatives</subject><subject>Genistein - pharmacology</subject><subject>Genistein - therapeutic use</subject><subject>Genotype & phenotype</subject><subject>Head injuries</subject><subject>IL-1β</subject><subject>Inflammation</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Ischemic Stroke - drug therapy</subject><subject>Ischemic Stroke - metabolism</subject><subject>Laboratories</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Mice</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglial cells</subject><subject>Neuroinflammatory Diseases - prevention & control</subject><subject>Neuroprotection</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Occlusion</subject><subject>Penicillin</subject><subject>Phosphorylation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion</subject><subject>Research Paper</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Sodium</subject><subject>Stroke</subject><subject>Sulfonates</subject><subject>Traumatic brain injury</subject><subject>Tumor necrosis factor-TNF</subject><subject>Veins & arteries</subject><issn>1449-2288</issn><issn>1449-2288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkUtuFDEQhi1ERMLAhgMgSyxASB3sdj83kYaBBKQkRBNYW9Xd7m4Pbjv4QTTcJkfINofImfAwIQqsXJK_-lVVH0IvKNkvaU7eyVXj9vOiIuQR2qNZVidpWlWPH9S76KlzK0JYkVfkCdplrCrKitE9dHUktHReSJ2w14kznQwTdkH1RoMXeO690CFWDp-KYI3UvYJpAi-NxlLjc2_Nd4GX4B1u1viDudTJUgxBRUIP-ES21gxKgsInFJ8ZBVb-2jb70ZowjPj2utTzxbhMTg-T25v3-FwOGtSm-Qz8eAnrZ2inB-XE87t3hr4dfvy6-JQcfzn6vJgfJy1LKUmaphOE9G3Niq7t2qZJGQWSll0Fdd3kUBJSV3Ft0VQko3nddx2DglBos7JrS8pm6GCbexGaSXSt0N6C4hdWTmDX3IDk__5oOfLB_OQxj7B42xl6cxdgzY8gnOeTdK1QCrQwwfE0j7KipbyM6Kv_0JUJNu69oeKYdV6mWaTebql4ROes6O-HoYRvzPONef7HfIRfPhz_Hv2rmv0GAaiuXQ</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Liu, Chaoming</creator><creator>Liu, Song</creator><creator>Xiong, Lijiao</creator><creator>Zhang, Limei</creator><creator>Li, Xiao</creator><creator>Cao, Xingling</creator><creator>Xue, Jinhua</creator><creator>Li, Liangdong</creator><creator>Huang, Cheng</creator><creator>Huang, Zhihua</creator><general>Ivyspring International Publisher Pty Ltd</general><general>Ivyspring International Publisher</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>7QL</scope><scope>7QO</scope><scope>7U9</scope><scope>8FD</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>2021</creationdate><title>Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway</title><author>Liu, Chaoming ; Liu, Song ; Xiong, Lijiao ; Zhang, Limei ; Li, Xiao ; Cao, Xingling ; Xue, Jinhua ; Li, Liangdong ; Huang, Cheng ; Huang, Zhihua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3210-bbde00fc936dcdcbb231a027d8a99b5a70098386eb804159fdd3a601ac47dc713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Animals</topic><topic>Blood-brain barrier</topic><topic>Brain</topic><topic>Brain Infarction - prevention & control</topic><topic>Brain injury</topic><topic>Cell Line</topic><topic>Cerebral blood flow</topic><topic>Cytokines</topic><topic>Depolarization</topic><topic>Drug Evaluation, Preclinical</topic><topic>Estrogens</topic><topic>Experiments</topic><topic>Genistein</topic><topic>Genistein - analogs & derivatives</topic><topic>Genistein - pharmacology</topic><topic>Genistein - therapeutic use</topic><topic>Genotype & phenotype</topic><topic>Head injuries</topic><topic>IL-1β</topic><topic>Inflammation</topic><topic>Injury prevention</topic><topic>Ischemia</topic><topic>Ischemic Stroke - drug therapy</topic><topic>Ischemic Stroke - metabolism</topic><topic>Laboratories</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglial cells</topic><topic>Neuroinflammatory Diseases - prevention & control</topic><topic>Neuroprotection</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Occlusion</topic><topic>Penicillin</topic><topic>Phosphorylation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion</topic><topic>Research Paper</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Sodium</topic><topic>Stroke</topic><topic>Sulfonates</topic><topic>Traumatic brain injury</topic><topic>Tumor necrosis factor-TNF</topic><topic>Veins & arteries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Chaoming</creatorcontrib><creatorcontrib>Liu, Song</creatorcontrib><creatorcontrib>Xiong, Lijiao</creatorcontrib><creatorcontrib>Zhang, Limei</creatorcontrib><creatorcontrib>Li, Xiao</creatorcontrib><creatorcontrib>Cao, Xingling</creatorcontrib><creatorcontrib>Xue, Jinhua</creatorcontrib><creatorcontrib>Li, Liangdong</creatorcontrib><creatorcontrib>Huang, Cheng</creatorcontrib><creatorcontrib>Huang, Zhihua</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Chaoming</au><au>Liu, Song</au><au>Xiong, Lijiao</au><au>Zhang, Limei</au><au>Li, Xiao</au><au>Cao, Xingling</au><au>Xue, Jinhua</au><au>Li, Liangdong</au><au>Huang, Cheng</au><au>Huang, Zhihua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway</atitle><jtitle>International journal of biological sciences</jtitle><addtitle>Int J Biol Sci</addtitle><date>2021</date><risdate>2021</risdate><volume>17</volume><issue>4</issue><spage>1088</spage><epage>1100</epage><pages>1088-1100</pages><issn>1449-2288</issn><eissn>1449-2288</eissn><abstract>Microglial M1 depolarization mediated prolonged inflammation contributing to brain injury in ischemic stroke. Our previous study revealed that Genistein-3'-sodium sulfonate (GSS) exerted neuroprotective effects in ischemic stroke. This study aimed to explore whether GSS protected against brain injury in ischemic stroke by regulating microglial M1 depolarization and its underlying mechanisms. We established transient middle cerebral artery occlusion and reperfusion (tMCAO) model in rats and used lipopolysaccharide (LPS)-stimulated BV2 microglial cells as
model. Our results showed that GSS treatment significantly reduced the brain infarcted volume and improved the neurological function in tMCAO rats. Meanwhile, GSS treatment also dramatically reduced microglia M1 depolarization and IL-1β level, reversed α7nAChR expression, and inhibited the activation of NF-κB signaling in the ischemic penumbra brain regions. These effects of GSS were further verified in LPS-induced M1 depolarization of BV2 cells. Furthermore, pretreatment of α7nAChR inhibitor (α-BTX) significantly restrained the neuroprotective effect of GSS treatment in tMCAO rats. α-BTX also blunted the regulating effects of GSS on neuroinflammation, M1 depolarization and NF-κB signaling activation. This study demonstrates that GSS protects against brain injury in ischemic stroke by reducing microglia M1 depolarization to suppress neuroinflammation in peri-infarcted brain regions through upregulating α7nAChR and thereby inhibition of NF-κB signaling. Our findings uncover a potential molecular mechanism for GSS treatment in ischemic stroke.</abstract><cop>Australia</cop><pub>Ivyspring International Publisher Pty Ltd</pub><pmid>33867831</pmid><doi>10.7150/ijbs.56800</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | alpha7 Nicotinic Acetylcholine Receptor - metabolism Animals Blood-brain barrier Brain Brain Infarction - prevention & control Brain injury Cell Line Cerebral blood flow Cytokines Depolarization Drug Evaluation, Preclinical Estrogens Experiments Genistein Genistein - analogs & derivatives Genistein - pharmacology Genistein - therapeutic use Genotype & phenotype Head injuries IL-1β Inflammation Injury prevention Ischemia Ischemic Stroke - drug therapy Ischemic Stroke - metabolism Laboratories Lipopolysaccharides Male Mice Microglia Microglia - drug effects Microglial cells Neuroinflammatory Diseases - prevention & control Neuroprotection NF-kappa B - metabolism NF-κB protein Occlusion Penicillin Phosphorylation Rats Rats, Sprague-Dawley Reperfusion Research Paper Signal transduction Signal Transduction - drug effects Signaling Sodium Stroke Sulfonates Traumatic brain injury Tumor necrosis factor-TNF Veins & arteries |
| title | Genistein-3'-sodium sulfonate Attenuates Neuroinflammation in Stroke Rats by Down-Regulating Microglial M1 Polarization through α7nAChR-NF-κB Signaling Pathway |
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