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Article: Neuropeptide Y-Y1 receptor modulates nitric oxide level during stroke in the rat

TitleNeuropeptide Y-Y1 receptor modulates nitric oxide level during stroke in the rat
Authors
KeywordsElectron paramagnetic resonance
Focal cerebral ischemia
Free radicals
Neuropeptide Y
Neuropeptide Y receptor
Nitric oxide
Issue Date2002
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology And Medicine, 2002, v. 32 n. 8, p. 776-784 How to Cite?
AbstractIn a rat endovascular middle cerebral artery occlusion (MCAO) stroke model, we previously showed that intracerebroventricular (ICV) injection of neuropeptide Y (NPY) or an Y1 receptor agonist, [Leu31,Pro34]-NPY, increased the infarct volume, that an Y1 receptor antagonist, BIBP3226, reduced the infarct volume, and that an Y2 receptor agonist, NPY3-36, had no effect. In this study, we used electron paramagnetic resonance (EPR) spectroscopy to measure nitric oxide (NO) and examined how ICV administration of NPY or its receptor analogs would modulate the brain NO level between the bregma levels +2 and -4 mm during MCAO, since excessive NO mediates ischemic damage. The relative brain NO concentration was increased to 131.94 ± 7.99% (mean ± SEM; n = 8) at 15 min of MCAO. NPY treatment further increased the relative brain NO concentration to 250.94 ± 50.48% (n = 8), whereas BIBP3226 significantly reduced the brain NO concentration to 69.63 ± 8.84% (n = 8). [Leu31,Pro34]-NPY (137.61 ± 14.54%; n = 7) or NPY3-36 (129.23 ± 21.77%; n = 8) did not affect the brain NO concentration at 15 min of MCAO. Our results suggest that the NPY-Y1 receptor activation mediates ischemic injury via NO overproduction and that inhibition of the Y1 receptor may confer protection via suppression of excessive NO production during ischemia. © 2002 Elsevier Science Inc.
Persistent Identifierhttp://hdl.handle.net/10722/78652
ISSN
2023 Impact Factor: 7.1
2023 SCImago Journal Rankings: 1.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, SHen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorCheung, RTFen_HK
dc.date.accessioned2010-09-06T07:45:15Z-
dc.date.available2010-09-06T07:45:15Z-
dc.date.issued2002en_HK
dc.identifier.citationFree Radical Biology And Medicine, 2002, v. 32 n. 8, p. 776-784en_HK
dc.identifier.issn0891-5849en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78652-
dc.description.abstractIn a rat endovascular middle cerebral artery occlusion (MCAO) stroke model, we previously showed that intracerebroventricular (ICV) injection of neuropeptide Y (NPY) or an Y1 receptor agonist, [Leu31,Pro34]-NPY, increased the infarct volume, that an Y1 receptor antagonist, BIBP3226, reduced the infarct volume, and that an Y2 receptor agonist, NPY3-36, had no effect. In this study, we used electron paramagnetic resonance (EPR) spectroscopy to measure nitric oxide (NO) and examined how ICV administration of NPY or its receptor analogs would modulate the brain NO level between the bregma levels +2 and -4 mm during MCAO, since excessive NO mediates ischemic damage. The relative brain NO concentration was increased to 131.94 ± 7.99% (mean ± SEM; n = 8) at 15 min of MCAO. NPY treatment further increased the relative brain NO concentration to 250.94 ± 50.48% (n = 8), whereas BIBP3226 significantly reduced the brain NO concentration to 69.63 ± 8.84% (n = 8). [Leu31,Pro34]-NPY (137.61 ± 14.54%; n = 7) or NPY3-36 (129.23 ± 21.77%; n = 8) did not affect the brain NO concentration at 15 min of MCAO. Our results suggest that the NPY-Y1 receptor activation mediates ischemic injury via NO overproduction and that inhibition of the Y1 receptor may confer protection via suppression of excessive NO production during ischemia. © 2002 Elsevier Science Inc.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_HK
dc.relation.ispartofFree Radical Biology and Medicineen_HK
dc.rightsFree Radical Biology & Medicine. Copyright © Elsevier Inc.en_HK
dc.subjectElectron paramagnetic resonance-
dc.subjectFocal cerebral ischemia-
dc.subjectFree radicals-
dc.subjectNeuropeptide Y-
dc.subjectNeuropeptide Y receptor-
dc.subjectNitric oxide-
dc.subject.meshAnimalsen_HK
dc.subject.meshArginine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshBrain - drug effectsen_HK
dc.subject.meshElectron Spin Resonance Spectroscopyen_HK
dc.subject.meshInjections, Intra-Arterialen_HK
dc.subject.meshInjections, Intraventricularen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNeuropeptide Y - pharmacologyen_HK
dc.subject.meshNitric Oxide - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReceptors, Neuropeptide Y - antagonists & inhibitors - metabolismen_HK
dc.subject.meshStroke - metabolism - pathologyen_HK
dc.titleNeuropeptide Y-Y1 receptor modulates nitric oxide level during stroke in the raten_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0891-5849&volume=32&spage=776&epage=784&date=2002&atitle=Neuropeptide+Y-Y1+receptor+modulates+nitric+oxide+level+during+stroke+in+the+raten_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0891-5849(02)00774-8en_HK
dc.identifier.pmid11937303en_HK
dc.identifier.scopuseid_2-s2.0-0037090113en_HK
dc.identifier.hkuros74441en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037090113&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume32en_HK
dc.identifier.issue8en_HK
dc.identifier.spage776en_HK
dc.identifier.epage784en_HK
dc.identifier.isiWOS:000175023700012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChen, SH=12806098400en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK
dc.identifier.issnl0891-5849-

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