Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3
No pharmacological treatment is currently available to protect brain from neuronal damage after ischemic stroke. Recent studies found that enkephalin may play an important role in neuron regeneration. We assembled a homogeneous size vesicle constituted by transferrin, exosomes, and enkephalin. Immun...
Gespeichert in:
Veröffentlicht in: | BioMed research international 2019-01, Vol.2019 (2019), p.1-11 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 11 |
---|---|
container_issue | 2019 |
container_start_page | 1 |
container_title | BioMed research international |
container_volume | 2019 |
creator | Wang, Xiumei Su, Jiangli Fu, Naisheng Liu, Yang Li, Xiaohua |
description | No pharmacological treatment is currently available to protect brain from neuronal damage after ischemic stroke. Recent studies found that enkephalin may play an important role in neuron regeneration. We assembled a homogeneous size vesicle constituted by transferrin, exosomes, and enkephalin. Immunofluorescence assay showed that transferrin was combined with the exosomes and enkephalin was packaged into the vesicle; thus this complex was called tar-exo-enkephalin. In vitro studies were performed using rat primary hippocampal neurons and the results showed that enkephalin decreased p53 and caspase-3 levels to 47.6% and 67.2%, respectively, compared to neurons treated with glutamate, thus inhibiting neuron apoptosis caused by glutamate. An in vivo experiment in rats was also carried out using a transient middle cerebral artery occlusion (tMCAO)/reperfusion model and tar-exo-enkephalin treatment was performed after tMCAO. The results showed that tar-exo-enkephalin crossed the blood brain barrier (BBB) and decreased the levels of LDH, p53, caspase-3, and NO by 41.9, 52.6, 45.5, and 57.9% compared to the tMCAO rats, respectively. In addition, tar-exo-enkephalin improved brain neuron density and neurological score after tMCAO. These findings suggest that the use of exogenous enkephalin might promote neurological recovery after stroke. |
doi_str_mv | 10.1155/2019/4273290 |
format | Article |
fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6425296</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A624417408</galeid><sourcerecordid>A624417408</sourcerecordid><originalsourceid>FETCH-LOGICAL-c565t-c46cf74af37e5dcedc4c93333cc6e9197f7904af6ec773bf2c244cdd9407b6a73</originalsourceid><addsrcrecordid>eNqNkc1v1DAQxSMEotXSG2dkiQsShPVX7PqCVC1bWKkCVOjZcpzJxm0Sp3ZSuhJ_PF522QIn5mJL85vneX5Z9pzgt4QUxZxiouacSkYVfpQdU0Z4Lggnjw93xo6ykxivcapTIrAST7MjhhVXBcbH2Y9LM7gKLfsbGBrTuh69h9bdQdigq-j6NVre--g7iGj06EvwnR8BfYIp-D6iS7D-F5rGVtE20DmLvo7B3wAqN2jVN65041ZlN2FaNBRsvjBxMBFy9ix7Ups2wsn-nGVX58tvi4_5xecPq8XZRW4LUYy55cLWkpuaSSgqC5XlVrFU1gpQRMlaKpzaAqyUrKyppZzbqlIcy1IYyWbZu53uMJVdGod-DKbVQ3CdCRvtjdN_d3rX6LW_04LTgiqRBF7tBYK_nSCOunPRQtuaHvwUNaWYC8XwKUvoy3_Qaz-FZD1RRLGUh1LygVqbFrTra5_etVtRfSbS9kTyJDbL3uwoG3yMAerDygTrbf56m7_e55_wF3_aPMC_007A6x3QuL4y391_ykFioDYPNEm_kpz8BBdLwZ4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2193133997</pqid></control><display><type>article</type><title>Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3</title><source>Wiley Online Library</source><source>PMC (PubMed Central)</source><source>Alma/SFX Local Collection</source><source>PubMed Central Open Access</source><creator>Wang, Xiumei ; Su, Jiangli ; Fu, Naisheng ; Liu, Yang ; Li, Xiaohua</creator><contributor>Rastaldo, Raffaella ; Raffaella Rastaldo</contributor><creatorcontrib>Wang, Xiumei ; Su, Jiangli ; Fu, Naisheng ; Liu, Yang ; Li, Xiaohua ; Rastaldo, Raffaella ; Raffaella Rastaldo</creatorcontrib><description>No pharmacological treatment is currently available to protect brain from neuronal damage after ischemic stroke. Recent studies found that enkephalin may play an important role in neuron regeneration. We assembled a homogeneous size vesicle constituted by transferrin, exosomes, and enkephalin. Immunofluorescence assay showed that transferrin was combined with the exosomes and enkephalin was packaged into the vesicle; thus this complex was called tar-exo-enkephalin. In vitro studies were performed using rat primary hippocampal neurons and the results showed that enkephalin decreased p53 and caspase-3 levels to 47.6% and 67.2%, respectively, compared to neurons treated with glutamate, thus inhibiting neuron apoptosis caused by glutamate. An in vivo experiment in rats was also carried out using a transient middle cerebral artery occlusion (tMCAO)/reperfusion model and tar-exo-enkephalin treatment was performed after tMCAO. The results showed that tar-exo-enkephalin crossed the blood brain barrier (BBB) and decreased the levels of LDH, p53, caspase-3, and NO by 41.9, 52.6, 45.5, and 57.9% compared to the tMCAO rats, respectively. In addition, tar-exo-enkephalin improved brain neuron density and neurological score after tMCAO. These findings suggest that the use of exogenous enkephalin might promote neurological recovery after stroke.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2019/4273290</identifier><identifier>PMID: 30949500</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animal experimentation ; Apoptosis ; Blood-brain barrier ; Brain ; Brain damage ; Brain injury ; Brain research ; Caspase ; Caspase-3 ; Cell culture ; Cerebral blood flow ; Drug therapy ; Enkephalins ; Exosomes ; Gene expression ; Glutamate ; Hippocampus ; Immunofluorescence ; Ischemia ; Metabolism ; Narcotics ; Neurons ; Neurosciences ; Occlusion ; p53 Protein ; Pharmacology ; Recovery ; Regeneration ; Reperfusion ; Stem cells ; Stroke ; Stroke (Disease) ; Tar ; Transferrin ; Transferrins ; Tumor proteins</subject><ispartof>BioMed research international, 2019-01, Vol.2019 (2019), p.1-11</ispartof><rights>Copyright © 2019 Yang Liu et al.</rights><rights>COPYRIGHT 2019 John Wiley & Sons, Inc.</rights><rights>Copyright © 2019 Yang Liu et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2019 Yang Liu et al. 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c565t-c46cf74af37e5dcedc4c93333cc6e9197f7904af6ec773bf2c244cdd9407b6a73</citedby><cites>FETCH-LOGICAL-c565t-c46cf74af37e5dcedc4c93333cc6e9197f7904af6ec773bf2c244cdd9407b6a73</cites><orcidid>0000-0002-9329-0814 ; 0000-0002-8011-3077</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425296/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425296/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30949500$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Rastaldo, Raffaella</contributor><contributor>Raffaella Rastaldo</contributor><creatorcontrib>Wang, Xiumei</creatorcontrib><creatorcontrib>Su, Jiangli</creatorcontrib><creatorcontrib>Fu, Naisheng</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Li, Xiaohua</creatorcontrib><title>Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>No pharmacological treatment is currently available to protect brain from neuronal damage after ischemic stroke. Recent studies found that enkephalin may play an important role in neuron regeneration. We assembled a homogeneous size vesicle constituted by transferrin, exosomes, and enkephalin. Immunofluorescence assay showed that transferrin was combined with the exosomes and enkephalin was packaged into the vesicle; thus this complex was called tar-exo-enkephalin. In vitro studies were performed using rat primary hippocampal neurons and the results showed that enkephalin decreased p53 and caspase-3 levels to 47.6% and 67.2%, respectively, compared to neurons treated with glutamate, thus inhibiting neuron apoptosis caused by glutamate. An in vivo experiment in rats was also carried out using a transient middle cerebral artery occlusion (tMCAO)/reperfusion model and tar-exo-enkephalin treatment was performed after tMCAO. The results showed that tar-exo-enkephalin crossed the blood brain barrier (BBB) and decreased the levels of LDH, p53, caspase-3, and NO by 41.9, 52.6, 45.5, and 57.9% compared to the tMCAO rats, respectively. In addition, tar-exo-enkephalin improved brain neuron density and neurological score after tMCAO. These findings suggest that the use of exogenous enkephalin might promote neurological recovery after stroke.</description><subject>Animal experimentation</subject><subject>Apoptosis</subject><subject>Blood-brain barrier</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Brain research</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>Cell culture</subject><subject>Cerebral blood flow</subject><subject>Drug therapy</subject><subject>Enkephalins</subject><subject>Exosomes</subject><subject>Gene expression</subject><subject>Glutamate</subject><subject>Hippocampus</subject><subject>Immunofluorescence</subject><subject>Ischemia</subject><subject>Metabolism</subject><subject>Narcotics</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Occlusion</subject><subject>p53 Protein</subject><subject>Pharmacology</subject><subject>Recovery</subject><subject>Regeneration</subject><subject>Reperfusion</subject><subject>Stem cells</subject><subject>Stroke</subject><subject>Stroke (Disease)</subject><subject>Tar</subject><subject>Transferrin</subject><subject>Transferrins</subject><subject>Tumor proteins</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc1v1DAQxSMEotXSG2dkiQsShPVX7PqCVC1bWKkCVOjZcpzJxm0Sp3ZSuhJ_PF522QIn5mJL85vneX5Z9pzgt4QUxZxiouacSkYVfpQdU0Z4Lggnjw93xo6ykxivcapTIrAST7MjhhVXBcbH2Y9LM7gKLfsbGBrTuh69h9bdQdigq-j6NVre--g7iGj06EvwnR8BfYIp-D6iS7D-F5rGVtE20DmLvo7B3wAqN2jVN65041ZlN2FaNBRsvjBxMBFy9ix7Ups2wsn-nGVX58tvi4_5xecPq8XZRW4LUYy55cLWkpuaSSgqC5XlVrFU1gpQRMlaKpzaAqyUrKyppZzbqlIcy1IYyWbZu53uMJVdGod-DKbVQ3CdCRvtjdN_d3rX6LW_04LTgiqRBF7tBYK_nSCOunPRQtuaHvwUNaWYC8XwKUvoy3_Qaz-FZD1RRLGUh1LygVqbFrTra5_etVtRfSbS9kTyJDbL3uwoG3yMAerDygTrbf56m7_e55_wF3_aPMC_007A6x3QuL4y391_ykFioDYPNEm_kpz8BBdLwZ4</recordid><startdate>20190101</startdate><enddate>20190101</enddate><creator>Wang, Xiumei</creator><creator>Su, Jiangli</creator><creator>Fu, Naisheng</creator><creator>Liu, Yang</creator><creator>Li, Xiaohua</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9329-0814</orcidid><orcidid>https://orcid.org/0000-0002-8011-3077</orcidid></search><sort><creationdate>20190101</creationdate><title>Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3</title><author>Wang, Xiumei ; Su, Jiangli ; Fu, Naisheng ; Liu, Yang ; Li, Xiaohua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c565t-c46cf74af37e5dcedc4c93333cc6e9197f7904af6ec773bf2c244cdd9407b6a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animal experimentation</topic><topic>Apoptosis</topic><topic>Blood-brain barrier</topic><topic>Brain</topic><topic>Brain damage</topic><topic>Brain injury</topic><topic>Brain research</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>Cell culture</topic><topic>Cerebral blood flow</topic><topic>Drug therapy</topic><topic>Enkephalins</topic><topic>Exosomes</topic><topic>Gene expression</topic><topic>Glutamate</topic><topic>Hippocampus</topic><topic>Immunofluorescence</topic><topic>Ischemia</topic><topic>Metabolism</topic><topic>Narcotics</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Occlusion</topic><topic>p53 Protein</topic><topic>Pharmacology</topic><topic>Recovery</topic><topic>Regeneration</topic><topic>Reperfusion</topic><topic>Stem cells</topic><topic>Stroke</topic><topic>Stroke (Disease)</topic><topic>Tar</topic><topic>Transferrin</topic><topic>Transferrins</topic><topic>Tumor proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Xiumei</creatorcontrib><creatorcontrib>Su, Jiangli</creatorcontrib><creatorcontrib>Fu, Naisheng</creatorcontrib><creatorcontrib>Liu, Yang</creatorcontrib><creatorcontrib>Li, Xiaohua</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - current)</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central</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>Biological Sciences</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>ProQuest advanced technologies & aerospace journals</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content (ProQuest)</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Xiumei</au><au>Su, Jiangli</au><au>Fu, Naisheng</au><au>Liu, Yang</au><au>Li, Xiaohua</au><au>Rastaldo, Raffaella</au><au>Raffaella Rastaldo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2019-01-01</date><risdate>2019</risdate><volume>2019</volume><issue>2019</issue><spage>1</spage><epage>11</epage><pages>1-11</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>No pharmacological treatment is currently available to protect brain from neuronal damage after ischemic stroke. Recent studies found that enkephalin may play an important role in neuron regeneration. We assembled a homogeneous size vesicle constituted by transferrin, exosomes, and enkephalin. Immunofluorescence assay showed that transferrin was combined with the exosomes and enkephalin was packaged into the vesicle; thus this complex was called tar-exo-enkephalin. In vitro studies were performed using rat primary hippocampal neurons and the results showed that enkephalin decreased p53 and caspase-3 levels to 47.6% and 67.2%, respectively, compared to neurons treated with glutamate, thus inhibiting neuron apoptosis caused by glutamate. An in vivo experiment in rats was also carried out using a transient middle cerebral artery occlusion (tMCAO)/reperfusion model and tar-exo-enkephalin treatment was performed after tMCAO. The results showed that tar-exo-enkephalin crossed the blood brain barrier (BBB) and decreased the levels of LDH, p53, caspase-3, and NO by 41.9, 52.6, 45.5, and 57.9% compared to the tMCAO rats, respectively. In addition, tar-exo-enkephalin improved brain neuron density and neurological score after tMCAO. These findings suggest that the use of exogenous enkephalin might promote neurological recovery after stroke.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30949500</pmid><doi>10.1155/2019/4273290</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-9329-0814</orcidid><orcidid>https://orcid.org/0000-0002-8011-3077</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2314-6133 |
ispartof | BioMed research international, 2019-01, Vol.2019 (2019), p.1-11 |
issn | 2314-6133 2314-6141 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6425296 |
source | Wiley Online Library; PMC (PubMed Central); Alma/SFX Local Collection; PubMed Central Open Access |
subjects | Animal experimentation Apoptosis Blood-brain barrier Brain Brain damage Brain injury Brain research Caspase Caspase-3 Cell culture Cerebral blood flow Drug therapy Enkephalins Exosomes Gene expression Glutamate Hippocampus Immunofluorescence Ischemia Metabolism Narcotics Neurons Neurosciences Occlusion p53 Protein Pharmacology Recovery Regeneration Reperfusion Stem cells Stroke Stroke (Disease) Tar Transferrin Transferrins Tumor proteins |
title | Rapid Enkephalin Delivery Using Exosomes to Promote Neurons Recovery in Ischemic Stroke by Inhibiting Neuronal p53/Caspase-3 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-04T19%3A31%3A27IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Rapid%20Enkephalin%20Delivery%20Using%20Exosomes%20to%20Promote%20Neurons%20Recovery%20in%20Ischemic%20Stroke%20by%20Inhibiting%20Neuronal%20p53/Caspase-3&rft.jtitle=BioMed%20research%20international&rft.au=Wang,%20Xiumei&rft.date=2019-01-01&rft.volume=2019&rft.issue=2019&rft.spage=1&rft.epage=11&rft.pages=1-11&rft.issn=2314-6133&rft.eissn=2314-6141&rft_id=info:doi/10.1155/2019/4273290&rft_dat=%3Cgale_pubme%3EA624417408%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2193133997&rft_id=info:pmid/30949500&rft_galeid=A624417408&rfr_iscdi=true |