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Article: Neuroprotective effects of lutein in a rat model of retinal detachment

TitleNeuroprotective effects of lutein in a rat model of retinal detachment
Authors
KeywordsApoptosis
Healon
Lutein
Neuroprotection
Retinal Detachment
Retinal Neuron
Xanthophyll
Issue Date2013
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00417/index.htm
Citation
Graefe's Archive For Clinical And Experimental Ophthalmology, 2013, v. 251 n. 1, p. 41-51 How to Cite?
AbstractBackground: Retinal detachment (RD) is a leading cause of blindness, and although final surgical re-attachment rate has greatly improved, visual outcome in many macula-off detachments is disappointing, mainly because of photoreceptor cell death. We previously showed that lutein is anti-apoptotic in rodent models of ischemia/reperfusion injury. The objective of this study is to investigate lutein as a possible pharmacological adjunct to surgery. Methods: Subretinal injections of 1.4 % sodium hyaluronate were used to induce RD in Sprague-Dawley rats until their retinae were approximately 70 % detached. Daily injections of corn oil (control group) or 0.5 mg/kg lutein in corn oil (treatment group) were given intraperitoneally starting 4 h after RD induction. Animals were euthanized 3 days and 30 days after RD and their retinae were analyzed for photoreceptor apoptosis and cell survival at the outer nuclear layer (ONL) using TUNEL staining and cell counting on retinal sections. Glial fibrillary acidic protein (GFAP) and rhodopsin (RHO) expression were evaluated with immunohistochemistry. Western blotting was done with antibodies against cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 to delineate lutein's mechanism of action in the apoptotic cascade. To seek a possible therapeutic time window, the same set of experiments was repeated with treatment commencing 36 h after RD. Results: When lutein was given 4 h after RD, there were significantly fewer TUNEL-positive cells in ONL 3 days after RD when compared with the vehicle group. Cell counting showed that there were significantly more nuclei in ONL in lutein-treated retinae by day 30. Treatment groups also showed significantly reduced GFAP immunoreactivity and preserved RHO expression. At day 3 after RD, Western blotting showed reduced expression of cleaved caspase-3 and cleaved caspase-8 in the treatment group. No difference was found for cleaved caspase-9. When lutein was given 36 h after RD similar results were observed. Conclusions: Our results suggest that lutein is a potent neuroprotective agent that can salvage photoreceptors in rats with RD, with a therapeutic window of at least 36 h. The use of lutein in patients with RD may serve as an adjunct to surgery to improve visual outcomes. © 2012 The Author(s).
Persistent Identifierhttp://hdl.handle.net/10722/176488
ISSN
2015 Impact Factor: 1.991
2015 SCImago Journal Rankings: 1.217
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWoo, TTYen_US
dc.contributor.authorLi, SYen_US
dc.contributor.authorLai, WWKen_US
dc.contributor.authorWong, Den_US
dc.contributor.authorLo, ACYen_US
dc.date.accessioned2012-11-26T09:11:44Z-
dc.date.available2012-11-26T09:11:44Z-
dc.date.issued2013en_US
dc.identifier.citationGraefe's Archive For Clinical And Experimental Ophthalmology, 2013, v. 251 n. 1, p. 41-51en_US
dc.identifier.issn0721-832Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/176488-
dc.description.abstractBackground: Retinal detachment (RD) is a leading cause of blindness, and although final surgical re-attachment rate has greatly improved, visual outcome in many macula-off detachments is disappointing, mainly because of photoreceptor cell death. We previously showed that lutein is anti-apoptotic in rodent models of ischemia/reperfusion injury. The objective of this study is to investigate lutein as a possible pharmacological adjunct to surgery. Methods: Subretinal injections of 1.4 % sodium hyaluronate were used to induce RD in Sprague-Dawley rats until their retinae were approximately 70 % detached. Daily injections of corn oil (control group) or 0.5 mg/kg lutein in corn oil (treatment group) were given intraperitoneally starting 4 h after RD induction. Animals were euthanized 3 days and 30 days after RD and their retinae were analyzed for photoreceptor apoptosis and cell survival at the outer nuclear layer (ONL) using TUNEL staining and cell counting on retinal sections. Glial fibrillary acidic protein (GFAP) and rhodopsin (RHO) expression were evaluated with immunohistochemistry. Western blotting was done with antibodies against cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9 to delineate lutein's mechanism of action in the apoptotic cascade. To seek a possible therapeutic time window, the same set of experiments was repeated with treatment commencing 36 h after RD. Results: When lutein was given 4 h after RD, there were significantly fewer TUNEL-positive cells in ONL 3 days after RD when compared with the vehicle group. Cell counting showed that there were significantly more nuclei in ONL in lutein-treated retinae by day 30. Treatment groups also showed significantly reduced GFAP immunoreactivity and preserved RHO expression. At day 3 after RD, Western blotting showed reduced expression of cleaved caspase-3 and cleaved caspase-8 in the treatment group. No difference was found for cleaved caspase-9. When lutein was given 36 h after RD similar results were observed. Conclusions: Our results suggest that lutein is a potent neuroprotective agent that can salvage photoreceptors in rats with RD, with a therapeutic window of at least 36 h. The use of lutein in patients with RD may serve as an adjunct to surgery to improve visual outcomes. © 2012 The Author(s).en_US
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00417/index.htmen_US
dc.relation.ispartofGraefe's Archive for Clinical and Experimental Ophthalmologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectApoptosisen_US
dc.subjectHealonen_US
dc.subjectLuteinen_US
dc.subjectNeuroprotectionen_US
dc.subjectRetinal Detachmenten_US
dc.subjectRetinal Neuronen_US
dc.subjectXanthophyllen_US
dc.titleNeuroprotective effects of lutein in a rat model of retinal detachmenten_US
dc.typeArticleen_US
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s00417-012-2128-zen_US
dc.identifier.pmid22899456-
dc.identifier.pmcidPMC3536954-
dc.identifier.scopuseid_2-s2.0-84872305154en_US
dc.identifier.hkuros223809-
dc.identifier.spage41en_US
dc.identifier.epage51en_US
dc.identifier.isiWOS:000313074100007-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridWoo, TTY=53265281800en_US
dc.identifier.scopusauthoridLi, SY=24329630700en_US
dc.identifier.scopusauthoridLai, WWK=55334321700en_US
dc.identifier.scopusauthoridWong, D=55323014200en_US
dc.identifier.scopusauthoridLo, ACY=7102780640en_US
dc.identifier.citeulike11130848-

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