File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Melatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice
  • Basic View
  • Metadata View
  • XML View
TitleMelatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice
 
AuthorsLiang, YZ1
Cheung, RTF1
Liu, S2
Li, G1
Huang, L2
 
Issue Date2006
 
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
 
CitationJournal Of Pineal Research, 2006, v. 41 n. 2, p. 150-156 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1600-079X.2006.00349.x
 
AbstractCyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24 and 48 hr after stroke. Cerebral blood flow (CBF) in the penumbra was monitored during stroke using a laser Doppler flowmeter. Sensorimotor behavior was evaluated using the turning in an alley and falling from a pole tests at 1 hr before stroke and 24 and 48 hr after stroke. Infarct volume was determined from the T2-weighted magnetic resonance images at 72 hr after stroke. During the first 15 min of stroke, CBF decreased in the penumbra in both homozygous COX-1-gene knockout and wild-type mice. Melatonin treatment improved the penumbral CBF in the wild-type mice. Mild poststroke impairment in sensorimotor behavior was detected by the turning in an alley test in which the COX-1-gene knockout mice performed better. Melatonin treatment did not affect the poststroke sensorimotor behavior. The relative infarct volume at 72 hr after stroke was 8.1% and 8.4% in the COX-1-gene knockout and wild-type mice, respectively. Melatonin treatment reduced the relative infarct volume to 6.3% in the latter but not in the former (8.2%). Thus, COX-1-gene knockout does not affect the brain's susceptibility to photothrombotic stroke. Melatonin treatment reduces infarct size in the wild-type mice following photothrombotic stroke partly via maintenance of penumbral CBF in which the COX-1-gene may play a role. © 2006 The Authors.
 
ISSN0742-3098
2013 Impact Factor: 7.812
 
DOIhttp://dx.doi.org/10.1111/j.1600-079X.2006.00349.x
 
ISI Accession Number IDWOS:000239371000009
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLiang, YZ
 
dc.contributor.authorCheung, RTF
 
dc.contributor.authorLiu, S
 
dc.contributor.authorLi, G
 
dc.contributor.authorHuang, L
 
dc.date.accessioned2010-09-06T07:41:53Z
 
dc.date.available2010-09-06T07:41:53Z
 
dc.date.issued2006
 
dc.description.abstractCyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24 and 48 hr after stroke. Cerebral blood flow (CBF) in the penumbra was monitored during stroke using a laser Doppler flowmeter. Sensorimotor behavior was evaluated using the turning in an alley and falling from a pole tests at 1 hr before stroke and 24 and 48 hr after stroke. Infarct volume was determined from the T2-weighted magnetic resonance images at 72 hr after stroke. During the first 15 min of stroke, CBF decreased in the penumbra in both homozygous COX-1-gene knockout and wild-type mice. Melatonin treatment improved the penumbral CBF in the wild-type mice. Mild poststroke impairment in sensorimotor behavior was detected by the turning in an alley test in which the COX-1-gene knockout mice performed better. Melatonin treatment did not affect the poststroke sensorimotor behavior. The relative infarct volume at 72 hr after stroke was 8.1% and 8.4% in the COX-1-gene knockout and wild-type mice, respectively. Melatonin treatment reduced the relative infarct volume to 6.3% in the latter but not in the former (8.2%). Thus, COX-1-gene knockout does not affect the brain's susceptibility to photothrombotic stroke. Melatonin treatment reduces infarct size in the wild-type mice following photothrombotic stroke partly via maintenance of penumbral CBF in which the COX-1-gene may play a role. © 2006 The Authors.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationJournal Of Pineal Research, 2006, v. 41 n. 2, p. 150-156 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1600-079X.2006.00349.x
 
dc.identifier.citeulike781038
 
dc.identifier.doihttp://dx.doi.org/10.1111/j.1600-079X.2006.00349.x
 
dc.identifier.epage156
 
dc.identifier.hkuros130496
 
dc.identifier.isiWOS:000239371000009
 
dc.identifier.issn0742-3098
2013 Impact Factor: 7.812
 
dc.identifier.issue2
 
dc.identifier.openurl
 
dc.identifier.pmid16879321
 
dc.identifier.scopuseid_2-s2.0-33746508995
 
dc.identifier.spage150
 
dc.identifier.urihttp://hdl.handle.net/10722/78349
 
dc.identifier.volume41
 
dc.languageeng
 
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
 
dc.publisher.placeDenmark
 
dc.relation.ispartofJournal of Pineal Research
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAnimals
 
dc.subject.meshBrain - blood supply - drug effects - pathology
 
dc.subject.meshBrain Edema - pathology
 
dc.subject.meshCerebral Infarction - drug therapy - pathology - physiopathology
 
dc.subject.meshCerebrovascular Circulation - drug effects
 
dc.subject.meshCyclooxygenase 1 - genetics
 
dc.subject.meshDisease Models, Animal
 
dc.subject.meshLaser-Doppler Flowmetry
 
dc.subject.meshMelatonin - administration & dosage - therapeutic use
 
dc.subject.meshMice
 
dc.subject.meshMice, Knockout
 
dc.subject.meshMotor Skills
 
dc.subject.meshNeuroprotective Agents - therapeutic use
 
dc.subject.meshReperfusion Injury - physiopathology
 
dc.subject.meshRose Bengal
 
dc.subject.meshThrombosis - metabolism
 
dc.titleMelatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Liang, YZ</contributor.author>
<contributor.author>Cheung, RTF</contributor.author>
<contributor.author>Liu, S</contributor.author>
<contributor.author>Li, G</contributor.author>
<contributor.author>Huang, L</contributor.author>
<date.accessioned>2010-09-06T07:41:53Z</date.accessioned>
<date.available>2010-09-06T07:41:53Z</date.available>
<date.issued>2006</date.issued>
<identifier.citation>Journal Of Pineal Research, 2006, v. 41 n. 2, p. 150-156</identifier.citation>
<identifier.issn>0742-3098</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/78349</identifier.uri>
<description.abstract>Cyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24 and 48 hr after stroke. Cerebral blood flow (CBF) in the penumbra was monitored during stroke using a laser Doppler flowmeter. Sensorimotor behavior was evaluated using the turning in an alley and falling from a pole tests at 1 hr before stroke and 24 and 48 hr after stroke. Infarct volume was determined from the T2-weighted magnetic resonance images at 72 hr after stroke. During the first 15 min of stroke, CBF decreased in the penumbra in both homozygous COX-1-gene knockout and wild-type mice. Melatonin treatment improved the penumbral CBF in the wild-type mice. Mild poststroke impairment in sensorimotor behavior was detected by the turning in an alley test in which the COX-1-gene knockout mice performed better. Melatonin treatment did not affect the poststroke sensorimotor behavior. The relative infarct volume at 72 hr after stroke was 8.1% and 8.4% in the COX-1-gene knockout and wild-type mice, respectively. Melatonin treatment reduced the relative infarct volume to 6.3% in the latter but not in the former (8.2%). Thus, COX-1-gene knockout does not affect the brain&apos;s susceptibility to photothrombotic stroke. Melatonin treatment reduces infarct size in the wild-type mice following photothrombotic stroke partly via maintenance of penumbral CBF in which the COX-1-gene may play a role. &#169; 2006 The Authors.</description.abstract>
<language>eng</language>
<publisher>Blackwell Munksgaard. The Journal&apos;s web site is located at http://www.blackwellpublishing.com/journals/JPI</publisher>
<relation.ispartof>Journal of Pineal Research</relation.ispartof>
<subject.mesh>Animals</subject.mesh>
<subject.mesh>Brain - blood supply - drug effects - pathology</subject.mesh>
<subject.mesh>Brain Edema - pathology</subject.mesh>
<subject.mesh>Cerebral Infarction - drug therapy - pathology - physiopathology</subject.mesh>
<subject.mesh>Cerebrovascular Circulation - drug effects</subject.mesh>
<subject.mesh>Cyclooxygenase 1 - genetics</subject.mesh>
<subject.mesh>Disease Models, Animal</subject.mesh>
<subject.mesh>Laser-Doppler Flowmetry</subject.mesh>
<subject.mesh>Melatonin - administration &amp; dosage - therapeutic use</subject.mesh>
<subject.mesh>Mice</subject.mesh>
<subject.mesh>Mice, Knockout</subject.mesh>
<subject.mesh>Motor Skills</subject.mesh>
<subject.mesh>Neuroprotective Agents - therapeutic use</subject.mesh>
<subject.mesh>Reperfusion Injury - physiopathology</subject.mesh>
<subject.mesh>Rose Bengal</subject.mesh>
<subject.mesh>Thrombosis - metabolism</subject.mesh>
<title>Melatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0742-3098&amp;volume=41&amp;spage=150&amp;epage=156&amp;date=2006&amp;atitle=Melatonin+reduces+infarction+volume+in+a+photothrombotic+stroke+model+in+the+wild-type+but+not+cyclooxygenase-1-gene+knockout+mice</identifier.openurl>
<description.nature>link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1111/j.1600-079X.2006.00349.x</identifier.doi>
<identifier.pmid>16879321</identifier.pmid>
<identifier.scopus>eid_2-s2.0-33746508995</identifier.scopus>
<identifier.hkuros>130496</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-33746508995&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>41</identifier.volume>
<identifier.issue>2</identifier.issue>
<identifier.spage>150</identifier.spage>
<identifier.epage>156</identifier.epage>
<identifier.isi>WOS:000239371000009</identifier.isi>
<publisher.place>Denmark</publisher.place>
<identifier.citeulike>781038</identifier.citeulike>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. Jinan University