File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Effect of lutein on retinal neurons and oxidative stress in a model of acute retinal ischemia/reperfusion

TitleEffect of lutein on retinal neurons and oxidative stress in a model of acute retinal ischemia/reperfusion
Authors
Issue Date2009
PublisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.org
Citation
Investigative Ophthalmology And Visual Science, 2009, v. 50 n. 2, p. 836-843 How to Cite?
AbstractPURPOSE. Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury. METHODS. Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR). RESULTS. In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In luteintreated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen. CONCLUSIONS. The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage. Copyright © Association for Research in Vision and Ophthalmology.
Persistent Identifierhttp://hdl.handle.net/10722/58231
ISSN
2015 Impact Factor: 3.427
2015 SCImago Journal Rankings: 2.008
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, SYen_HK
dc.contributor.authorFu, ZJen_HK
dc.contributor.authorMa, Hen_HK
dc.contributor.authorJang, WCen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorWong, Den_HK
dc.contributor.authorLo, ACYen_HK
dc.date.accessioned2010-05-31T03:26:16Z-
dc.date.available2010-05-31T03:26:16Z-
dc.date.issued2009en_HK
dc.identifier.citationInvestigative Ophthalmology And Visual Science, 2009, v. 50 n. 2, p. 836-843en_HK
dc.identifier.issn0146-0404en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58231-
dc.description.abstractPURPOSE. Retinal ischemia/reperfusion (I/R) occurs in many ocular diseases and leads to neuronal death. Lutein, a potent antioxidant, is used to prevent severe visual loss in patients with early age-related macular degeneration (AMD), but its effect on I/R insult is unclear. The objective of the present study is to investigate the neuroprotective effect of lutein on retinal neurons after acute I/R injury. METHODS. Unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein or vehicle was administered. The number of viable retinal ganglion cells (RGC) was quantified. Apoptosis was investigated using TUNEL assay. Oxidative stress was elucidated using markers such as nitrotyrosine (NT) and poly(ADP-ribose) (PAR). RESULTS. In vehicle-treated I/R retina, severe cell loss in ganglion cell layer, increased apoptosis as well as increased NT and nuclear PAR immunoreactivity were observed. In luteintreated I/R retina, significantly less cell loss, decreased number of apoptotic cells, and decreased NT and nuclear PAR immunoreactivity were seen. CONCLUSIONS. The neuroprotective effect of lutein was associated with reduced oxidative stress. Lutein has been hitherto used principally for protection of outer retinal elements in AMD. Our study suggests that it may also be relevant for the protection of inner retina from acute ischemic damage. Copyright © Association for Research in Vision and Ophthalmology.en_HK
dc.languageengen_HK
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.orgen_HK
dc.relation.ispartofInvestigative Ophthalmology and Visual Scienceen_HK
dc.subject.meshAntioxidants - pharmacology-
dc.subject.meshOxidative Stress - drug effects-
dc.subject.meshReperfusion Injury - metabolism - pathology - prevention and control-
dc.subject.meshRetinal Diseases - metabolism - pathology - prevention and control-
dc.subject.meshRetinal Ganglion Cells - drug effects - pathology-
dc.titleEffect of lutein on retinal neurons and oxidative stress in a model of acute retinal ischemia/reperfusionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0146-0404&volume=50&issue=2&spage=836&epage=843&date=2009&atitle=Effect+of+lutein+on+retinal+neurons+and+oxidative+stress+in+a+model+of+acute+retinal+ischemia/reperfusion-
dc.identifier.emailSo, KF: hrmaskf@hku.hken_HK
dc.identifier.emailWong, D: shdwong@hku.hken_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityWong, D=rp00516en_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1167/iovs.08-2310en_HK
dc.identifier.pmid18936152en_HK
dc.identifier.scopuseid_2-s2.0-59449098831en_HK
dc.identifier.hkuros154564en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-59449098831&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume50en_HK
dc.identifier.issue2en_HK
dc.identifier.spage836en_HK
dc.identifier.epage843en_HK
dc.identifier.eissn1552-5783-
dc.identifier.isiWOS:000262665900046-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, SY=24329630700en_HK
dc.identifier.scopusauthoridFu, ZJ=36908915500en_HK
dc.identifier.scopusauthoridMa, H=35722659800en_HK
dc.identifier.scopusauthoridJang, WC=26026313600en_HK
dc.identifier.scopusauthoridSo, KF=34668391300en_HK
dc.identifier.scopusauthoridWong, D=7401536078en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats