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Therapeutic time window for the neuroprotective effects of NGF when administered after focal cerebral ischemia
In the present study, we evaluated the neuroprotection time window for nerve growth factor (NGF) after ischemia/reperfusion brain injury in rabbits as related to this anti-apoptosis mechanism. Male New Zealand rabbits were subjected to 2 h of middle cerebral artery occlusion (MCAO), followed by 70 h...
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| Published in: | Neurological sciences 2011-06, Vol.32 (3), p.433-441 |
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| Main Authors: | , , , |
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| Language: | English |
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| cites | cdi_FETCH-LOGICAL-c468t-392c0e414c432aeacbd200eebebf039052b6b7b6222d1b5b218b82b74b3918153 |
| container_end_page | 441 |
| container_issue | 3 |
| container_start_page | 433 |
| container_title | Neurological sciences |
| container_volume | 32 |
| creator | Yang, Ji-Ping Liu, Huai-Jun Yang, Hua Feng, Ping-Yong |
| description | In the present study, we evaluated the neuroprotection time window for nerve growth factor (NGF) after ischemia/reperfusion brain injury in rabbits as related to this anti-apoptosis mechanism. Male New Zealand rabbits were subjected to 2 h of middle cerebral artery occlusion (MCAO), followed by 70 h of reperfusion. NGF was administered after injury to evaluate the time window. Neurological deficits, infarct volume, neural cell apoptosis and expressions of caspase-3 and Bcl-2 were measured. Compared to saline-treated control, NGF treatment at 2, 3 and 5 h after MCAO significantly reduced infarct volume, neural cell apoptosis and expression of caspase-3 (
P
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| doi_str_mv | 10.1007/s10072-011-0512-9 |
| format | article |
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P
< 0.01), up-regulated the expression of Bcl-2 and improved functional recovery (
P
< 0.01). However, treatment at latter time points did not produce significant neuroprotection. Neuroprotection treatment with NGF provides an extended time window of up to 5 h after ischemia/reperfusion brain injury, in part by attenuating the apoptosis.</description><identifier>ISSN: 1590-1874</identifier><identifier>EISSN: 1590-3478</identifier><identifier>DOI: 10.1007/s10072-011-0512-9</identifier><identifier>PMID: 21409508</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Animals ; Brain Ischemia - drug therapy ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Disease Models, Animal ; Drug Administration Schedule ; Injections, Intraventricular ; Male ; Medicine ; Medicine & Public Health ; Nerve Growth Factor - administration & dosage ; Nerve Growth Factor - physiology ; Neurology ; Neuroprotective Agents - administration & dosage ; Neuroprotective Agents - pharmacology ; Neuroradiology ; Neurosciences ; Neurosurgery ; Original Article ; Psychiatry ; Rabbits ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Time Factors</subject><ispartof>Neurological sciences, 2011-06, Vol.32 (3), p.433-441</ispartof><rights>Springer-Verlag 2011</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-392c0e414c432aeacbd200eebebf039052b6b7b6222d1b5b218b82b74b3918153</citedby><cites>FETCH-LOGICAL-c468t-392c0e414c432aeacbd200eebebf039052b6b7b6222d1b5b218b82b74b3918153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21409508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Ji-Ping</creatorcontrib><creatorcontrib>Liu, Huai-Jun</creatorcontrib><creatorcontrib>Yang, Hua</creatorcontrib><creatorcontrib>Feng, Ping-Yong</creatorcontrib><title>Therapeutic time window for the neuroprotective effects of NGF when administered after focal cerebral ischemia</title><title>Neurological sciences</title><addtitle>Neurol Sci</addtitle><addtitle>Neurol Sci</addtitle><description>In the present study, we evaluated the neuroprotection time window for nerve growth factor (NGF) after ischemia/reperfusion brain injury in rabbits as related to this anti-apoptosis mechanism. Male New Zealand rabbits were subjected to 2 h of middle cerebral artery occlusion (MCAO), followed by 70 h of reperfusion. NGF was administered after injury to evaluate the time window. Neurological deficits, infarct volume, neural cell apoptosis and expressions of caspase-3 and Bcl-2 were measured. Compared to saline-treated control, NGF treatment at 2, 3 and 5 h after MCAO significantly reduced infarct volume, neural cell apoptosis and expression of caspase-3 (
P
< 0.01), up-regulated the expression of Bcl-2 and improved functional recovery (
P
< 0.01). However, treatment at latter time points did not produce significant neuroprotection. Neuroprotection treatment with NGF provides an extended time window of up to 5 h after ischemia/reperfusion brain injury, in part by attenuating the apoptosis.</description><subject>Animals</subject><subject>Brain Ischemia - drug therapy</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Disease Models, Animal</subject><subject>Drug Administration Schedule</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nerve Growth Factor - administration & dosage</subject><subject>Nerve Growth Factor - physiology</subject><subject>Neurology</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroradiology</subject><subject>Neurosciences</subject><subject>Neurosurgery</subject><subject>Original Article</subject><subject>Psychiatry</subject><subject>Rabbits</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Time Factors</subject><issn>1590-1874</issn><issn>1590-3478</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqFkU9P3DAQxS1Exb_2A3CpLC6cQmccJ7GPCAFFQvRCz5btTFijTbK1E1Z8e7zabSshIS6ekf17b8Z6jJ0iXCBA8yNtTlEAYgEVikLvsSOsNBSlbNT-rkfVyEN2nNIzAKDE8oAdCpSgK1BHbHhcULQrmqfg-RR64uswtOOad2Pk04L4QHMcV3GcyE_hhTh1Xe4SHzv-cHvD1wsauG37MIQ0UaSW2y7XLPd2yX2-cTE3IfkF9cF-ZV86u0z0bVdP2O-b68ern8X9r9u7q8v7wstaTUWphQeSKL0shSXrXSsAiBy5DkoNlXC1a1wthGjRVU6gckq4RrpSo8KqPGHnW9-8-Z-Z0mT6vAItl3agcU5GNbUoGxT4OVnXlVAa6kyevSOfxzkO-RvZrtFS62pjh1vIxzGlSJ1ZxdDb-GoQzCYusw3N5NDMJjSjs-b7znh2PbX_FH9TyoDYAik_DU8U_0_-2PUN4yWh5A</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Yang, Ji-Ping</creator><creator>Liu, Huai-Jun</creator><creator>Yang, Hua</creator><creator>Feng, Ping-Yong</creator><general>Springer Milan</general><general>Springer Nature B.V</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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20110601</creationdate><title>Therapeutic time window for the neuroprotective effects of NGF when administered after focal cerebral ischemia</title><author>Yang, Ji-Ping ; 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Male New Zealand rabbits were subjected to 2 h of middle cerebral artery occlusion (MCAO), followed by 70 h of reperfusion. NGF was administered after injury to evaluate the time window. Neurological deficits, infarct volume, neural cell apoptosis and expressions of caspase-3 and Bcl-2 were measured. Compared to saline-treated control, NGF treatment at 2, 3 and 5 h after MCAO significantly reduced infarct volume, neural cell apoptosis and expression of caspase-3 (
P
< 0.01), up-regulated the expression of Bcl-2 and improved functional recovery (
P
< 0.01). However, treatment at latter time points did not produce significant neuroprotection. Neuroprotection treatment with NGF provides an extended time window of up to 5 h after ischemia/reperfusion brain injury, in part by attenuating the apoptosis.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>21409508</pmid><doi>10.1007/s10072-011-0512-9</doi><tpages>9</tpages></addata></record> |
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| ispartof | Neurological sciences, 2011-06, Vol.32 (3), p.433-441 |
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| source | Springer Nature:Jisc Collections:Springer Nature Read and Publish 2023-2025: Springer Reading List |
| subjects | Animals Brain Ischemia - drug therapy Brain Ischemia - metabolism Brain Ischemia - pathology Disease Models, Animal Drug Administration Schedule Injections, Intraventricular Male Medicine Medicine & Public Health Nerve Growth Factor - administration & dosage Nerve Growth Factor - physiology Neurology Neuroprotective Agents - administration & dosage Neuroprotective Agents - pharmacology Neuroradiology Neurosciences Neurosurgery Original Article Psychiatry Rabbits Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Time Factors |
| title | Therapeutic time window for the neuroprotective effects of NGF when administered after focal cerebral ischemia |
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