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Article: The effect of low-energy laser irradiation on apoptotic factors following experimentally induced transient cerebral ischemia

TitleThe effect of low-energy laser irradiation on apoptotic factors following experimentally induced transient cerebral ischemia
Authors
KeywordsApoptosis
Caspase
Ischemia
Laser
Stroke
Issue Date2011
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 2011, v. 190, p. 301-306 How to Cite?
AbstractApoptosis, or programmed cell death, resulting from cerebral ischemia may be related to decreased levels of anti-apoptotic factors, such as serine/threonine kinase (Akt), phosphorylated Akt (pAkt), pBAD, and Bcl-2, and increased levels of pro-apoptotic factors, such as BAD, caspase 9, and caspase 3 activities. In this study, we investigated the effects of low-energy laser (660 nm) irradiation (LLI) on the levels and activity of various anti- and pro-apoptotic factors following ischemia. Transient cerebral ischemia was induced in Sprague-Dawley rats by unilateral occlusion of the middle cerebral artery for 1 h, followed by reperfusion. LLI was then directed on the cerebrum for varying lengths of duration (1, 5, or 10 min at an energy density of 2.64 J/cm 2, 13.2 J/cm 2, and 24.6 J/cm 2, respectively). The expression levels of Akt, pAkt, BAD, pBAD, Bcl-2, caspase 9, and caspase 3 activities were measured 4 days after injury. The levels of Akt, pAkt, Bcl-2, and pBAD were significantly increased following laser irradiation. In addition, LLI significantly decreased caspase 9 and caspase 3 activities caused by ischemia-reperfusion. LLI may protect the brain by upregulating Akt, pAkt, pBAD, and Bcl-2 expression and downregulating caspase 9 and caspase 3 expression following transient cerebral ischemia. This modality is a promising protective therapeutic intervention after strokes or other ischemic events. © 2011 IBRO.
Persistent Identifierhttp://hdl.handle.net/10722/142321
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Polytechnic UniversityJBB71
BB8V
Funding Information:

This research was supported by Niche Area Grant (JBB71 & BB8V) from the Hong Kong Polytechnic University. The authors thank Ms. Christine Van and Dr. Joe Ching for editing.

References

 

DC FieldValueLanguage
dc.contributor.authorYip, KKen_HK
dc.contributor.authorLo, SCLen_HK
dc.contributor.authorLeung, MCPen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorTang, CYen_HK
dc.contributor.authorPoon, DMYen_HK
dc.date.accessioned2011-10-28T02:42:50Z-
dc.date.available2011-10-28T02:42:50Z-
dc.date.issued2011en_HK
dc.identifier.citationNeuroscience, 2011, v. 190, p. 301-306en_HK
dc.identifier.issn0306-4522en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142321-
dc.description.abstractApoptosis, or programmed cell death, resulting from cerebral ischemia may be related to decreased levels of anti-apoptotic factors, such as serine/threonine kinase (Akt), phosphorylated Akt (pAkt), pBAD, and Bcl-2, and increased levels of pro-apoptotic factors, such as BAD, caspase 9, and caspase 3 activities. In this study, we investigated the effects of low-energy laser (660 nm) irradiation (LLI) on the levels and activity of various anti- and pro-apoptotic factors following ischemia. Transient cerebral ischemia was induced in Sprague-Dawley rats by unilateral occlusion of the middle cerebral artery for 1 h, followed by reperfusion. LLI was then directed on the cerebrum for varying lengths of duration (1, 5, or 10 min at an energy density of 2.64 J/cm 2, 13.2 J/cm 2, and 24.6 J/cm 2, respectively). The expression levels of Akt, pAkt, BAD, pBAD, Bcl-2, caspase 9, and caspase 3 activities were measured 4 days after injury. The levels of Akt, pAkt, Bcl-2, and pBAD were significantly increased following laser irradiation. In addition, LLI significantly decreased caspase 9 and caspase 3 activities caused by ischemia-reperfusion. LLI may protect the brain by upregulating Akt, pAkt, pBAD, and Bcl-2 expression and downregulating caspase 9 and caspase 3 expression following transient cerebral ischemia. This modality is a promising protective therapeutic intervention after strokes or other ischemic events. © 2011 IBRO.en_HK
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscienceen_HK
dc.relation.ispartofNeuroscienceen_HK
dc.subjectApoptosisen_HK
dc.subjectCaspaseen_HK
dc.subjectIschemiaen_HK
dc.subjectLaseren_HK
dc.subjectStrokeen_HK
dc.titleThe effect of low-energy laser irradiation on apoptotic factors following experimentally induced transient cerebral ischemiaen_HK
dc.typeArticleen_HK
dc.identifier.emailSo, KF:hrmaskf@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.neuroscience.2011.06.022en_HK
dc.identifier.pmid21712070-
dc.identifier.scopuseid_2-s2.0-80051593311en_HK
dc.identifier.hkuros197678en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051593311&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume190en_HK
dc.identifier.spage301en_HK
dc.identifier.epage306en_HK
dc.identifier.isiWOS:000294878800029-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridYip, KK=49462021300en_HK
dc.identifier.scopusauthoridLo, SCL=7401542305en_HK
dc.identifier.scopusauthoridLeung, MCP=7201943351en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridTang, CY=7404394088en_HK
dc.identifier.scopusauthoridPoon, DMY=36855939400en_HK
dc.identifier.citeulike9488550-

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