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Article: Treatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up-regulates the expression of transforming growth factor-beta 1

TitleTreatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up-regulates the expression of transforming growth factor-beta 1
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34073
Citation
Lasers In Surgery And Medicine, 2002, v. 31 n. 4, p. 283-288 How to Cite?
AbstractBackground and Objectives: Nitric oxide (NO) has been shown to be neurotoxic while transforming growth factor-beta 1 (TGF-β1) is neuroprotective in the stroke model. The present study investigates the effects of low energy laser on nitric oxide synthase (NOS) and TGF-β1 activities after cerebral ischemia and reperfusion injury. Study Design/Materials and Methods: Cerebral ischemia was induced for 1 hour in male adult Sprague-Dawley (S.D.) rats with unilateral occlusion of middle cerebral artery (MCAO). Low energy laser irradiation was then applied to the cerebrum at different durations (1, 5, or 10 minutes). The activity of NOS and the expression of TGF-β1 were evaluated in groups with different durations of laser irradiation. Results: After ischemia, the activity of NOS was gradually increased from day 3, became significantly higher from day 4 to 6 (P < 0.001), but returned to the normal level after day 7. The activity and expression of the three isoforms of NOS were significantly suppressed (P < 0.001) to different extents after laser irradiation. In addition, laser irradiation was shown to trigger the expression of TGF-β1 (P < 0.001). Conclusions: Low energy laser could suppress the activity of NOS and up-regulate the expression of TGF-β1 after stroke in rats. © 2002 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67942
ISSN
2015 Impact Factor: 2.135
2015 SCImago Journal Rankings: 0.977
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, MCPen_HK
dc.contributor.authorLo, SCLen_HK
dc.contributor.authorSiu, FKWen_HK
dc.contributor.authorSo, KFen_HK
dc.date.accessioned2010-09-06T05:59:40Z-
dc.date.available2010-09-06T05:59:40Z-
dc.date.issued2002en_HK
dc.identifier.citationLasers In Surgery And Medicine, 2002, v. 31 n. 4, p. 283-288en_HK
dc.identifier.issn0196-8092en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67942-
dc.description.abstractBackground and Objectives: Nitric oxide (NO) has been shown to be neurotoxic while transforming growth factor-beta 1 (TGF-β1) is neuroprotective in the stroke model. The present study investigates the effects of low energy laser on nitric oxide synthase (NOS) and TGF-β1 activities after cerebral ischemia and reperfusion injury. Study Design/Materials and Methods: Cerebral ischemia was induced for 1 hour in male adult Sprague-Dawley (S.D.) rats with unilateral occlusion of middle cerebral artery (MCAO). Low energy laser irradiation was then applied to the cerebrum at different durations (1, 5, or 10 minutes). The activity of NOS and the expression of TGF-β1 were evaluated in groups with different durations of laser irradiation. Results: After ischemia, the activity of NOS was gradually increased from day 3, became significantly higher from day 4 to 6 (P < 0.001), but returned to the normal level after day 7. The activity and expression of the three isoforms of NOS were significantly suppressed (P < 0.001) to different extents after laser irradiation. In addition, laser irradiation was shown to trigger the expression of TGF-β1 (P < 0.001). Conclusions: Low energy laser could suppress the activity of NOS and up-regulate the expression of TGF-β1 after stroke in rats. © 2002 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34073en_HK
dc.relation.ispartofLasers in Surgery and Medicineen_HK
dc.rightsLasers in Surgery and Medicine. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshIschemic Attack, Transient - physiopathology - radiotherapyen_HK
dc.subject.meshLaser Therapy, Low-Levelen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Cerebral Artery - physiopathology - radiation effectsen_HK
dc.subject.meshNitric Oxide Synthase - physiology - radiation effectsen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Sprague-Dawleyen_HK
dc.subject.meshReperfusion Injury - physiopathology - radiotherapyen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTransforming Growth Factor beta - analysis - radiation effectsen_HK
dc.subject.meshTransforming Growth Factor beta1en_HK
dc.subject.meshUp-Regulation - physiology - radiation effectsen_HK
dc.titleTreatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up-regulates the expression of transforming growth factor-beta 1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0196-8092&volume=31&spage=283&epage=288&date=2002&atitle=Treatment+of+experimentally+induced+transient+cerebral+ischemia+with+low+energy+laser+inhibits+nitric+oxide+synthase+activity+and+up-regulates+the+expression+of+transforming+growth+factor-beta+1en_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/lsm.10096en_HK
dc.identifier.pmid12355575-
dc.identifier.scopuseid_2-s2.0-0036398802en_HK
dc.identifier.hkuros74637en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036398802&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue4en_HK
dc.identifier.spage283en_HK
dc.identifier.epage288en_HK
dc.identifier.isiWOS:000178649100011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLeung, MCP=7201943351en_HK
dc.identifier.scopusauthoridLo, SCL=7401542305en_HK
dc.identifier.scopusauthoridSiu, FKW=6701518486en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK

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