Ginkgetin Promotes M2 Polarization of Microglia and Exert Neuroprotection in Ischemic Stroke via Modulation of PPARγ Pathway
Neuroinflammation plays an important role in the pathophysiological process of acute cerebral infarction, which may aggravate brain injury and hinder neuro-repair. Microglia are innate immune cells in the brain. Ginkgetin has anti-inflammatory and neuroprotective effects, but the mechanism remains u...
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description | Neuroinflammation plays an important role in the pathophysiological process of acute cerebral infarction, which may aggravate brain injury and hinder neuro-repair. Microglia are innate immune cells in the brain. Ginkgetin has anti-inflammatory and neuroprotective effects, but the mechanism remains unclear. This study aims to explore the regulatory effects of ginkgetin on microglia polarization in brain ischemia. Oxygen glucose deprivation (OGD) cellular model and middle cerebral artery occlusion (MCAO) animal model was used in this study. We first observed the dynamic process of microglia polarization in ischemic stroke, and then investigated the effect of ginkgetin treatment on microglia polarization. Finally, we studied the role of PPARγ signaling pathway and the blocking effect of PPARγ antagonist GW9662 in this process. OGD and cerebral ischemia polarized microglia mainly to M1 type. However, ginkgetin treatment converted microglia from M1 type to M2 type, inhibited neuroinflammation, and exerted neuronal protective effects. PPARγ signaling pathway was activated during this process. The above effects could be blocked by GW9662. Ginkgetin can promote M2 polarization of microglia through PPARγ signaling pathway, thereby inhibiting neuroinflammation and promoting recovery of neurological functions in ischemic stroke. |
doi_str_mv | 10.1007/s11064-022-03583-3 |
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Microglia are innate immune cells in the brain. Ginkgetin has anti-inflammatory and neuroprotective effects, but the mechanism remains unclear. This study aims to explore the regulatory effects of ginkgetin on microglia polarization in brain ischemia. Oxygen glucose deprivation (OGD) cellular model and middle cerebral artery occlusion (MCAO) animal model was used in this study. We first observed the dynamic process of microglia polarization in ischemic stroke, and then investigated the effect of ginkgetin treatment on microglia polarization. Finally, we studied the role of PPARγ signaling pathway and the blocking effect of PPARγ antagonist GW9662 in this process. OGD and cerebral ischemia polarized microglia mainly to M1 type. However, ginkgetin treatment converted microglia from M1 type to M2 type, inhibited neuroinflammation, and exerted neuronal protective effects. PPARγ signaling pathway was activated during this process. The above effects could be blocked by GW9662. Ginkgetin can promote M2 polarization of microglia through PPARγ signaling pathway, thereby inhibiting neuroinflammation and promoting recovery of neurological functions in ischemic stroke.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-022-03583-3</identifier><identifier>PMID: 35593977</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain ; Brain injury ; Cell Biology ; Cerebral blood flow ; Cerebral infarction ; Deprivation ; Head injuries ; Immune system ; Inflammation ; Ischemia ; Microglia ; Neurochemistry ; Neurology ; Neuromodulation ; Neuroprotection ; Neurosciences ; Occlusion ; Original Paper ; Peroxisome proliferator-activated receptors ; Polarization ; Signal transduction ; Signaling ; Stroke</subject><ispartof>Neurochemical research, 2022-10, Vol.47 (10), p.2963-2974</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022</rights><rights>2022. 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Microglia are innate immune cells in the brain. Ginkgetin has anti-inflammatory and neuroprotective effects, but the mechanism remains unclear. This study aims to explore the regulatory effects of ginkgetin on microglia polarization in brain ischemia. Oxygen glucose deprivation (OGD) cellular model and middle cerebral artery occlusion (MCAO) animal model was used in this study. We first observed the dynamic process of microglia polarization in ischemic stroke, and then investigated the effect of ginkgetin treatment on microglia polarization. Finally, we studied the role of PPARγ signaling pathway and the blocking effect of PPARγ antagonist GW9662 in this process. OGD and cerebral ischemia polarized microglia mainly to M1 type. However, ginkgetin treatment converted microglia from M1 type to M2 type, inhibited neuroinflammation, and exerted neuronal protective effects. PPARγ signaling pathway was activated during this process. The above effects could be blocked by GW9662. Ginkgetin can promote M2 polarization of microglia through PPARγ signaling pathway, thereby inhibiting neuroinflammation and promoting recovery of neurological functions in ischemic stroke.</description><subject>Animal models</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain</subject><subject>Brain injury</subject><subject>Cell Biology</subject><subject>Cerebral blood flow</subject><subject>Cerebral infarction</subject><subject>Deprivation</subject><subject>Head injuries</subject><subject>Immune system</subject><subject>Inflammation</subject><subject>Ischemia</subject><subject>Microglia</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neuromodulation</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>Occlusion</subject><subject>Original Paper</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Polarization</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stroke</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1u1TAQRi0EopfCC7BAltiwCYw9sZ0sq6otlXoh4mdtObmTW7dJXOwEKBJPxXvwTJjeUiQWrLyY830ezWHsqYCXAsC8SkKALguQsgBUFRZ4j62EMljoGvA-WwHmMYoa9tijlC4AckyKh2wPlaqxNmbFvp_46XJLs594E8MYZkp8LXkTBhf9Nzf7MPHQ87XvYtgO3nE3bfjRV4ozf0NLDFcxR7obLFecpu6cRt_x93MMl8Q_58A6bJbhrqhpDt79_MEbN59_cdeP2YPeDYme3L777OPx0YfD18XZ25PTw4OzokOj5qJ1ZdWqttxIUQvVCk2oNJW9cAocGUNGOEAnVavbnrpeknYlVVRBXZeAgPvsxa43r_tpoTTb0aeOhsFNFJZkpdbGVEobndHn_6AXYYlT3s5KI7DSgMZkSu6ofJaUIvX2KvrRxWsrwP6WY3dybJZjb-RYzKFnt9VLO9LmLvLHRgZwB6Q8mrYU__79n9pfrlWbKQ</recordid><startdate>20221001</startdate><enddate>20221001</enddate><creator>Tang, Tianchi</creator><creator>Wang, Xiongwei</creator><creator>Qi, Enbo</creator><creator>Li, Shiting</creator><creator>Sun, Hui</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20221001</creationdate><title>Ginkgetin Promotes M2 Polarization of Microglia and Exert Neuroprotection in Ischemic Stroke via Modulation of PPARγ Pathway</title><author>Tang, Tianchi ; Wang, Xiongwei ; Qi, Enbo ; Li, Shiting ; Sun, Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-ba48b5b4d21915b16e356e4f1a50ae77e71a03a25b6bfecf2e6a4e8e809940303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animal models</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain</topic><topic>Brain injury</topic><topic>Cell Biology</topic><topic>Cerebral blood flow</topic><topic>Cerebral infarction</topic><topic>Deprivation</topic><topic>Head injuries</topic><topic>Immune system</topic><topic>Inflammation</topic><topic>Ischemia</topic><topic>Microglia</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neuromodulation</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>Occlusion</topic><topic>Original Paper</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Polarization</topic><topic>Signal transduction</topic><topic>Signaling</topic><topic>Stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Tianchi</creatorcontrib><creatorcontrib>Wang, Xiongwei</creatorcontrib><creatorcontrib>Qi, Enbo</creatorcontrib><creatorcontrib>Li, Shiting</creatorcontrib><creatorcontrib>Sun, Hui</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Tianchi</au><au>Wang, Xiongwei</au><au>Qi, Enbo</au><au>Li, Shiting</au><au>Sun, Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ginkgetin Promotes M2 Polarization of Microglia and Exert Neuroprotection in Ischemic Stroke via Modulation of PPARγ Pathway</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2022-10-01</date><risdate>2022</risdate><volume>47</volume><issue>10</issue><spage>2963</spage><epage>2974</epage><pages>2963-2974</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Neuroinflammation plays an important role in the pathophysiological process of acute cerebral infarction, which may aggravate brain injury and hinder neuro-repair. Microglia are innate immune cells in the brain. Ginkgetin has anti-inflammatory and neuroprotective effects, but the mechanism remains unclear. This study aims to explore the regulatory effects of ginkgetin on microglia polarization in brain ischemia. Oxygen glucose deprivation (OGD) cellular model and middle cerebral artery occlusion (MCAO) animal model was used in this study. We first observed the dynamic process of microglia polarization in ischemic stroke, and then investigated the effect of ginkgetin treatment on microglia polarization. Finally, we studied the role of PPARγ signaling pathway and the blocking effect of PPARγ antagonist GW9662 in this process. OGD and cerebral ischemia polarized microglia mainly to M1 type. However, ginkgetin treatment converted microglia from M1 type to M2 type, inhibited neuroinflammation, and exerted neuronal protective effects. PPARγ signaling pathway was activated during this process. The above effects could be blocked by GW9662. Ginkgetin can promote M2 polarization of microglia through PPARγ signaling pathway, thereby inhibiting neuroinflammation and promoting recovery of neurological functions in ischemic stroke.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35593977</pmid><doi>10.1007/s11064-022-03583-3</doi><tpages>12</tpages></addata></record> |
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subjects | Animal models Biochemistry Biomedical and Life Sciences Biomedicine Brain Brain injury Cell Biology Cerebral blood flow Cerebral infarction Deprivation Head injuries Immune system Inflammation Ischemia Microglia Neurochemistry Neurology Neuromodulation Neuroprotection Neurosciences Occlusion Original Paper Peroxisome proliferator-activated receptors Polarization Signal transduction Signaling Stroke |
title | Ginkgetin Promotes M2 Polarization of Microglia and Exert Neuroprotection in Ischemic Stroke via Modulation of PPARγ Pathway |
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