The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons
The neuroprotective role of propofol in transient global and focal cerebral ischemia reperfusion (I/R) animal model has recently been highlighted. However, no studies have conducted to explore the relationship between mitochondrial fission/fusion and I/R injury under the intervention of propofol. Mo...
Gespeichert in:
| Veröffentlicht in: | PloS one 2016-10, Vol.11 (10), p.e0165052-e0165052 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0165052 |
|---|---|
| container_issue | 10 |
| container_start_page | e0165052 |
| container_title | PloS one |
| container_volume | 11 |
| creator | Wang, Haibin Zheng, Shengfa Liu, Maodong Jia, Changxin Wang, Shilei Wang, Xue Xue, Sha Guo, Yunliang |
| description | The neuroprotective role of propofol in transient global and focal cerebral ischemia reperfusion (I/R) animal model has recently been highlighted. However, no studies have conducted to explore the relationship between mitochondrial fission/fusion and I/R injury under the intervention of propofol. Moreover, neuroprotective mechanism of propofol is yet unclear. Culturing primary hippocampal cells were subjected to oxygen-glucose deprivation and re-oxygenation (OGD/R) model, as a model of cerebral I/R in vitro. Methods CCK-8 assay was used to test the effect of propofol on cell viability. We examined the effect of propofol on mitochondrial ultrastructure and mitochondrial fission evoked by OGD/R with transmission electron microscopy and immunofluorescence assay. To investigate possible neuroprotective mechanisms, the authors then examined whether propofol could inhibit calcium-overload, calcineurin (CaN) activation and the phosphorylation of dynamin-related protein 1 (Drp1) during the period of OGD/R, as well as the combination of Drp1-ser 637 and fission 1 (Fis1) protein by immunofluorescence assay, ELISA and double-labeling immunofluorescence analysis. Finally, the expression of Drp1-ser 637 and Fis1, apoptosis inducing factor (AIF) and cytochrome C (Cyt C) were detected by western blot. When added in culture media during OGD period, propofol (0.1μM-50μM) could alleviate neurons injury and protect mitochondrial ultrastructure, meanwhile inhibit mitochondrial fission. Furthermore, the concentration of intracellular free Ca2+, CaN activition and the phosphorylation of Drp1-ser637 were suppressed, as well as the translocation and combination of Drp1-ser 637 and Fis1. The authors also found that the expression of Cyt C, AIF, Drp1-ser637 and Fis1 were down-regulated. Notably, high dose of propofol (100μM-200μM) were confirmed to decrease the survival of neurons based on results of cell viability. Propofol could inhibit mitochondrial fission and mitochondrial apoptotic pathway evoked by OGD/R in rat hippocampal neurons, which may be via depressing calcium-overload. |
| doi_str_mv | 10.1371/journal.pone.0165052 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1833129549</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A471908263</galeid><doaj_id>oai_doaj_org_article_f3c2b26f53b546708283995abe92f0df</doaj_id><sourcerecordid>A471908263</sourcerecordid><originalsourceid>FETCH-LOGICAL-c791t-1cd9c1a79965b5cfc497fa62e53482c5b5d964900edf8ba6d58e968729faa283</originalsourceid><addsrcrecordid>eNqNk11v0zAUhiMEYmPwDxBEQkJw0eKP2I5vkKaxj0qDolJxazmO3bpK7WAn03bNH8dts6lFu5h8Yev4eV8fH_tk2VsIxhAz-GXl--BkM26902MAKQEEPcuOIcdoRBHAz_fWR9mrGFcAEFxS-jI7QoyVJWTsOPs7X-r83Bitutyb_GfwrTe-yb3Lv9vOq6V3dbCyyS9sjDZF6z5Yt8int3cL7UaXTa981Pk33QZ7I7sNIV2dz3Srg-m3iolb9eEuty6fyS6_sm3rlVy3yfOH7oN38XX2wsgm6jfDfJLNL87nZ1ej6-nl5Oz0eqQYh90IqporKBnnlFREGVVwZiRFmuCiRCrFak4LDoCuTVlJWpNSc1oyxI2UqMQn2fudbdv4KIbyRQFLjCHipOCJmOyI2suVSDday3AnvLRiG_BhIWTorGq0MFihClFDcEUKykCZDuCcyEpzZEBtktfX4bS-WutaadcF2RyYHu44uxQLfyPI1gskg0-DQfB_eh07sbZR6aaRTvt-mzfDgMMSPQUllJUEb9AP_6GPF2KgFjLd1TrjU4pqYypOCwZ5SpHiRI0fodKo9dqq9C2NTfEDwecDQWI6fdstZB-jmPyaPZ2d_j5kP-6xSy2bbhl902--YzwEix2ogo8xaPPwHhCITVfdV0NsukoMXZVk7_bf8kF030b4H1QVHZU</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1833129549</pqid></control><display><type>article</type><title>The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Public Library of Science (PLoS)</source><creator>Wang, Haibin ; Zheng, Shengfa ; Liu, Maodong ; Jia, Changxin ; Wang, Shilei ; Wang, Xue ; Xue, Sha ; Guo, Yunliang</creator><creatorcontrib>Wang, Haibin ; Zheng, Shengfa ; Liu, Maodong ; Jia, Changxin ; Wang, Shilei ; Wang, Xue ; Xue, Sha ; Guo, Yunliang</creatorcontrib><description>The neuroprotective role of propofol in transient global and focal cerebral ischemia reperfusion (I/R) animal model has recently been highlighted. However, no studies have conducted to explore the relationship between mitochondrial fission/fusion and I/R injury under the intervention of propofol. Moreover, neuroprotective mechanism of propofol is yet unclear. Culturing primary hippocampal cells were subjected to oxygen-glucose deprivation and re-oxygenation (OGD/R) model, as a model of cerebral I/R in vitro. Methods CCK-8 assay was used to test the effect of propofol on cell viability. We examined the effect of propofol on mitochondrial ultrastructure and mitochondrial fission evoked by OGD/R with transmission electron microscopy and immunofluorescence assay. To investigate possible neuroprotective mechanisms, the authors then examined whether propofol could inhibit calcium-overload, calcineurin (CaN) activation and the phosphorylation of dynamin-related protein 1 (Drp1) during the period of OGD/R, as well as the combination of Drp1-ser 637 and fission 1 (Fis1) protein by immunofluorescence assay, ELISA and double-labeling immunofluorescence analysis. Finally, the expression of Drp1-ser 637 and Fis1, apoptosis inducing factor (AIF) and cytochrome C (Cyt C) were detected by western blot. When added in culture media during OGD period, propofol (0.1μM-50μM) could alleviate neurons injury and protect mitochondrial ultrastructure, meanwhile inhibit mitochondrial fission. Furthermore, the concentration of intracellular free Ca2+, CaN activition and the phosphorylation of Drp1-ser637 were suppressed, as well as the translocation and combination of Drp1-ser 637 and Fis1. The authors also found that the expression of Cyt C, AIF, Drp1-ser637 and Fis1 were down-regulated. Notably, high dose of propofol (100μM-200μM) were confirmed to decrease the survival of neurons based on results of cell viability. Propofol could inhibit mitochondrial fission and mitochondrial apoptotic pathway evoked by OGD/R in rat hippocampal neurons, which may be via depressing calcium-overload.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0165052</identifier><identifier>PMID: 27788177</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Anesthesia ; Anesthesiology ; Animals ; Apoptosis ; Apoptosis-inducing factor ; Assaying ; Biology and Life Sciences ; Calcineurin ; Calcium ; Calcium (intracellular) ; Calcium - metabolism ; Calcium ions ; Cell culture ; Cell survival ; Cell Survival - drug effects ; Cells, Cultured ; Cholecystokinin ; Culture media ; Cytochrome ; Cytochrome c ; Deprivation ; Dynamin ; Electron microscopy ; Enzyme-linked immunosorbent assay ; Fission ; Glucose ; Glucose - deficiency ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - physiopathology ; Hippocampus - ultrastructure ; Hospitals ; Hypoxia - drug therapy ; Immunofluorescence ; In vitro methods and tests ; Injuries ; Ischemia ; Kinases ; Media (culture) ; Medicine and Health Sciences ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - ultrastructure ; Mitochondrial Dynamics - drug effects ; Neurons ; Neuroprotection ; Oxygen ; Oxygenation ; Permeability ; Phenols (Class of compounds) ; Phosphorylation ; Propofol ; Propofol - pharmacology ; Rats ; Rats, Sprague-Dawley ; Reperfusion ; Reperfusion Injury - prevention & control ; Research and Analysis Methods ; Rodents ; Translocation ; Transmission electron microscopy ; Traumatic brain injury ; Ultrastructure</subject><ispartof>PloS one, 2016-10, Vol.11 (10), p.e0165052-e0165052</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Wang et al 2016 Wang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c791t-1cd9c1a79965b5cfc497fa62e53482c5b5d964900edf8ba6d58e968729faa283</citedby><cites>FETCH-LOGICAL-c791t-1cd9c1a79965b5cfc497fa62e53482c5b5d964900edf8ba6d58e968729faa283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082830/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5082830/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27788177$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Haibin</creatorcontrib><creatorcontrib>Zheng, Shengfa</creatorcontrib><creatorcontrib>Liu, Maodong</creatorcontrib><creatorcontrib>Jia, Changxin</creatorcontrib><creatorcontrib>Wang, Shilei</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Xue, Sha</creatorcontrib><creatorcontrib>Guo, Yunliang</creatorcontrib><title>The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The neuroprotective role of propofol in transient global and focal cerebral ischemia reperfusion (I/R) animal model has recently been highlighted. However, no studies have conducted to explore the relationship between mitochondrial fission/fusion and I/R injury under the intervention of propofol. Moreover, neuroprotective mechanism of propofol is yet unclear. Culturing primary hippocampal cells were subjected to oxygen-glucose deprivation and re-oxygenation (OGD/R) model, as a model of cerebral I/R in vitro. Methods CCK-8 assay was used to test the effect of propofol on cell viability. We examined the effect of propofol on mitochondrial ultrastructure and mitochondrial fission evoked by OGD/R with transmission electron microscopy and immunofluorescence assay. To investigate possible neuroprotective mechanisms, the authors then examined whether propofol could inhibit calcium-overload, calcineurin (CaN) activation and the phosphorylation of dynamin-related protein 1 (Drp1) during the period of OGD/R, as well as the combination of Drp1-ser 637 and fission 1 (Fis1) protein by immunofluorescence assay, ELISA and double-labeling immunofluorescence analysis. Finally, the expression of Drp1-ser 637 and Fis1, apoptosis inducing factor (AIF) and cytochrome C (Cyt C) were detected by western blot. When added in culture media during OGD period, propofol (0.1μM-50μM) could alleviate neurons injury and protect mitochondrial ultrastructure, meanwhile inhibit mitochondrial fission. Furthermore, the concentration of intracellular free Ca2+, CaN activition and the phosphorylation of Drp1-ser637 were suppressed, as well as the translocation and combination of Drp1-ser 637 and Fis1. The authors also found that the expression of Cyt C, AIF, Drp1-ser637 and Fis1 were down-regulated. Notably, high dose of propofol (100μM-200μM) were confirmed to decrease the survival of neurons based on results of cell viability. Propofol could inhibit mitochondrial fission and mitochondrial apoptotic pathway evoked by OGD/R in rat hippocampal neurons, which may be via depressing calcium-overload.</description><subject>Anesthesia</subject><subject>Anesthesiology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis-inducing factor</subject><subject>Assaying</subject><subject>Biology and Life Sciences</subject><subject>Calcineurin</subject><subject>Calcium</subject><subject>Calcium (intracellular)</subject><subject>Calcium - metabolism</subject><subject>Calcium ions</subject><subject>Cell culture</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Cells, Cultured</subject><subject>Cholecystokinin</subject><subject>Culture media</subject><subject>Cytochrome</subject><subject>Cytochrome c</subject><subject>Deprivation</subject><subject>Dynamin</subject><subject>Electron microscopy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fission</subject><subject>Glucose</subject><subject>Glucose - deficiency</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - physiopathology</subject><subject>Hippocampus - ultrastructure</subject><subject>Hospitals</subject><subject>Hypoxia - drug therapy</subject><subject>Immunofluorescence</subject><subject>In vitro methods and tests</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Media (culture)</subject><subject>Medicine and Health Sciences</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - ultrastructure</subject><subject>Mitochondrial Dynamics - drug effects</subject><subject>Neurons</subject><subject>Neuroprotection</subject><subject>Oxygen</subject><subject>Oxygenation</subject><subject>Permeability</subject><subject>Phenols (Class of compounds)</subject><subject>Phosphorylation</subject><subject>Propofol</subject><subject>Propofol - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Research and Analysis Methods</subject><subject>Rodents</subject><subject>Translocation</subject><subject>Transmission electron microscopy</subject><subject>Traumatic brain injury</subject><subject>Ultrastructure</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11v0zAUhiMEYmPwDxBEQkJw0eKP2I5vkKaxj0qDolJxazmO3bpK7WAn03bNH8dts6lFu5h8Yev4eV8fH_tk2VsIxhAz-GXl--BkM26902MAKQEEPcuOIcdoRBHAz_fWR9mrGFcAEFxS-jI7QoyVJWTsOPs7X-r83Bitutyb_GfwrTe-yb3Lv9vOq6V3dbCyyS9sjDZF6z5Yt8int3cL7UaXTa981Pk33QZ7I7sNIV2dz3Srg-m3iolb9eEuty6fyS6_sm3rlVy3yfOH7oN38XX2wsgm6jfDfJLNL87nZ1ej6-nl5Oz0eqQYh90IqporKBnnlFREGVVwZiRFmuCiRCrFak4LDoCuTVlJWpNSc1oyxI2UqMQn2fudbdv4KIbyRQFLjCHipOCJmOyI2suVSDday3AnvLRiG_BhIWTorGq0MFihClFDcEUKykCZDuCcyEpzZEBtktfX4bS-WutaadcF2RyYHu44uxQLfyPI1gskg0-DQfB_eh07sbZR6aaRTvt-mzfDgMMSPQUllJUEb9AP_6GPF2KgFjLd1TrjU4pqYypOCwZ5SpHiRI0fodKo9dqq9C2NTfEDwecDQWI6fdstZB-jmPyaPZ2d_j5kP-6xSy2bbhl902--YzwEix2ogo8xaPPwHhCITVfdV0NsukoMXZVk7_bf8kF030b4H1QVHZU</recordid><startdate>20161027</startdate><enddate>20161027</enddate><creator>Wang, Haibin</creator><creator>Zheng, Shengfa</creator><creator>Liu, Maodong</creator><creator>Jia, Changxin</creator><creator>Wang, Shilei</creator><creator>Wang, Xue</creator><creator>Xue, Sha</creator><creator>Guo, Yunliang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20161027</creationdate><title>The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons</title><author>Wang, Haibin ; Zheng, Shengfa ; Liu, Maodong ; Jia, Changxin ; Wang, Shilei ; Wang, Xue ; Xue, Sha ; Guo, Yunliang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c791t-1cd9c1a79965b5cfc497fa62e53482c5b5d964900edf8ba6d58e968729faa283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Anesthesia</topic><topic>Anesthesiology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis-inducing factor</topic><topic>Assaying</topic><topic>Biology and Life Sciences</topic><topic>Calcineurin</topic><topic>Calcium</topic><topic>Calcium (intracellular)</topic><topic>Calcium - metabolism</topic><topic>Calcium ions</topic><topic>Cell culture</topic><topic>Cell survival</topic><topic>Cell Survival - drug effects</topic><topic>Cells, Cultured</topic><topic>Cholecystokinin</topic><topic>Culture media</topic><topic>Cytochrome</topic><topic>Cytochrome c</topic><topic>Deprivation</topic><topic>Dynamin</topic><topic>Electron microscopy</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fission</topic><topic>Glucose</topic><topic>Glucose - deficiency</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - physiopathology</topic><topic>Hippocampus - ultrastructure</topic><topic>Hospitals</topic><topic>Hypoxia - drug therapy</topic><topic>Immunofluorescence</topic><topic>In vitro methods and tests</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Media (culture)</topic><topic>Medicine and Health Sciences</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - ultrastructure</topic><topic>Mitochondrial Dynamics - drug effects</topic><topic>Neurons</topic><topic>Neuroprotection</topic><topic>Oxygen</topic><topic>Oxygenation</topic><topic>Permeability</topic><topic>Phenols (Class of compounds)</topic><topic>Phosphorylation</topic><topic>Propofol</topic><topic>Propofol - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Research and Analysis Methods</topic><topic>Rodents</topic><topic>Translocation</topic><topic>Transmission electron microscopy</topic><topic>Traumatic brain injury</topic><topic>Ultrastructure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Haibin</creatorcontrib><creatorcontrib>Zheng, Shengfa</creatorcontrib><creatorcontrib>Liu, Maodong</creatorcontrib><creatorcontrib>Jia, Changxin</creatorcontrib><creatorcontrib>Wang, Shilei</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Xue, Sha</creatorcontrib><creatorcontrib>Guo, Yunliang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Haibin</au><au>Zheng, Shengfa</au><au>Liu, Maodong</au><au>Jia, Changxin</au><au>Wang, Shilei</au><au>Wang, Xue</au><au>Xue, Sha</au><au>Guo, Yunliang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-10-27</date><risdate>2016</risdate><volume>11</volume><issue>10</issue><spage>e0165052</spage><epage>e0165052</epage><pages>e0165052-e0165052</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The neuroprotective role of propofol in transient global and focal cerebral ischemia reperfusion (I/R) animal model has recently been highlighted. However, no studies have conducted to explore the relationship between mitochondrial fission/fusion and I/R injury under the intervention of propofol. Moreover, neuroprotective mechanism of propofol is yet unclear. Culturing primary hippocampal cells were subjected to oxygen-glucose deprivation and re-oxygenation (OGD/R) model, as a model of cerebral I/R in vitro. Methods CCK-8 assay was used to test the effect of propofol on cell viability. We examined the effect of propofol on mitochondrial ultrastructure and mitochondrial fission evoked by OGD/R with transmission electron microscopy and immunofluorescence assay. To investigate possible neuroprotective mechanisms, the authors then examined whether propofol could inhibit calcium-overload, calcineurin (CaN) activation and the phosphorylation of dynamin-related protein 1 (Drp1) during the period of OGD/R, as well as the combination of Drp1-ser 637 and fission 1 (Fis1) protein by immunofluorescence assay, ELISA and double-labeling immunofluorescence analysis. Finally, the expression of Drp1-ser 637 and Fis1, apoptosis inducing factor (AIF) and cytochrome C (Cyt C) were detected by western blot. When added in culture media during OGD period, propofol (0.1μM-50μM) could alleviate neurons injury and protect mitochondrial ultrastructure, meanwhile inhibit mitochondrial fission. Furthermore, the concentration of intracellular free Ca2+, CaN activition and the phosphorylation of Drp1-ser637 were suppressed, as well as the translocation and combination of Drp1-ser 637 and Fis1. The authors also found that the expression of Cyt C, AIF, Drp1-ser637 and Fis1 were down-regulated. Notably, high dose of propofol (100μM-200μM) were confirmed to decrease the survival of neurons based on results of cell viability. Propofol could inhibit mitochondrial fission and mitochondrial apoptotic pathway evoked by OGD/R in rat hippocampal neurons, which may be via depressing calcium-overload.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27788177</pmid><doi>10.1371/journal.pone.0165052</doi><tpages>e0165052</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-10, Vol.11 (10), p.e0165052-e0165052 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1833129549 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Anesthesia Anesthesiology Animals Apoptosis Apoptosis-inducing factor Assaying Biology and Life Sciences Calcineurin Calcium Calcium (intracellular) Calcium - metabolism Calcium ions Cell culture Cell survival Cell Survival - drug effects Cells, Cultured Cholecystokinin Culture media Cytochrome Cytochrome c Deprivation Dynamin Electron microscopy Enzyme-linked immunosorbent assay Fission Glucose Glucose - deficiency Hippocampus Hippocampus - drug effects Hippocampus - physiopathology Hippocampus - ultrastructure Hospitals Hypoxia - drug therapy Immunofluorescence In vitro methods and tests Injuries Ischemia Kinases Media (culture) Medicine and Health Sciences Mitochondria Mitochondria - drug effects Mitochondria - ultrastructure Mitochondrial Dynamics - drug effects Neurons Neuroprotection Oxygen Oxygenation Permeability Phenols (Class of compounds) Phosphorylation Propofol Propofol - pharmacology Rats Rats, Sprague-Dawley Reperfusion Reperfusion Injury - prevention & control Research and Analysis Methods Rodents Translocation Transmission electron microscopy Traumatic brain injury Ultrastructure |
| title | The Effect of Propofol on Mitochondrial Fission during Oxygen-Glucose Deprivation and Reperfusion Injury in Rat Hippocampal Neurons |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T14%3A32%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20Effect%20of%20Propofol%20on%20Mitochondrial%20Fission%20during%20Oxygen-Glucose%20Deprivation%20and%20Reperfusion%20Injury%20in%20Rat%20Hippocampal%20Neurons&rft.jtitle=PloS%20one&rft.au=Wang,%20Haibin&rft.date=2016-10-27&rft.volume=11&rft.issue=10&rft.spage=e0165052&rft.epage=e0165052&rft.pages=e0165052-e0165052&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0165052&rft_dat=%3Cgale_plos_%3EA471908263%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1833129549&rft_id=info:pmid/27788177&rft_galeid=A471908263&rft_doaj_id=oai_doaj_org_article_f3c2b26f53b546708283995abe92f0df&rfr_iscdi=true |