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Conference Paper: Lutein preserved retinal function and minimized inflammatory response in retinal ischemia/reperfusion injury

TitleLutein preserved retinal function and minimized inflammatory response in retinal ischemia/reperfusion injury
Authors
KeywordsRetinal Ganglion Cell
Eye
Glia
Issue Date2013
PublisherAmerican Society of Neuroscience.
Citation
The 42nd Annual Meeting of the Society for Neuroscience (SfN), New Orleans, USA, 13-17 October 2012 How to Cite?
AbstractPURPOSE. Retinal ischemia/reperfusion (I/R) injury is a feature of ocular pathologies such as amaurosis fugax and acute angle-closure glaucoma, leading to irreversible neuronal damage and visual impairment. Our previous studies showed that lutein is neuroprotective in retinal I/R injury. Besides being anti-apoptotic and anti-oxidative, lutein is also implicated to be anti-inflammatory. As Müller cell plays a critical role in inflammation in retinal diseases, the effect of lutein on Müller cells was investigated in a mouse retinal I/R injury model and a chemical-induced hypoxia cell culture model. METHODS. Male C57Bl/6N mice were challenged with 2-hour retinal ischemia followed by 22-hour reperfusion by intraluminal blockade of the internal carotid artery that provides blood supply to the eye. Lutein (0.2mg/kg) or vehicle (10% DMSO) was administered by intraperitoneal injection at 1 hour before and 1 hour after reperfusion. Electroretinography (ERG) and GFAP immunoreactivity were examined in retinal sections. On the other hand, in vitro hypoxia was induced in a retinal Müller cell line (rMC-1) with cobalt (II) chloride. Western blotting of IL-1β, Cox-2, TNFα, and NFκB were then performed to assess the effect of lutein administration. RESULTS. With lutein post-treatment, the deterioration in ERG response and the activation of retinal GFAP were minimized in the animal model of retinal I/R injury. In the cell culture model of hypoxia, lutein administration decreased the levels of IL-1β, Cox-2 and nuclear NFκB but not TNFα. CONCLUSIONS. Lutein post-treatment preserved retinal function and reduced Müller cell gliosis after retinal I/R injury. The reduction of inflammatory factor production from Müller cells after lutein administration suggested an anti-inflammatory role of lutein. Together with our previous studies, these results indicate that lutein protects the retina from I/R damage by its anti-oxidative, anti-apoptotic and anti-inflammatory properties, making lutein an attractive therapeutic agent in eye diseases in which acute ischemia is a feature.
DescriptionPoster session 765: Ischemia: Neuroprotection III
Program#765.11 & Poster#S6
Fulltext of the abstract in: http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=723bcad0-3faa-4500-88f6-f25fc9a16aec&cKey=4d9b71ed-f96d-4b2a-9696-1d611a2e0c72&mKey=%7b70007181-01C9-4DE9-A0A2-EEBFA14CD9F1%7d
Persistent Identifierhttp://hdl.handle.net/10722/191089

 

DC FieldValueLanguage
dc.contributor.authorLo, ACYen_US
dc.contributor.authorLi, SYen_US
dc.contributor.authorFung, KCFen_US
dc.contributor.authorChan, HHen_US
dc.contributor.authorWong, DSHen_US
dc.date.accessioned2013-09-17T16:15:43Z-
dc.date.available2013-09-17T16:15:43Z-
dc.date.issued2013en_US
dc.identifier.citationThe 42nd Annual Meeting of the Society for Neuroscience (SfN), New Orleans, USA, 13-17 October 2012en_US
dc.identifier.urihttp://hdl.handle.net/10722/191089-
dc.descriptionPoster session 765: Ischemia: Neuroprotection III-
dc.descriptionProgram#765.11 & Poster#S6-
dc.descriptionFulltext of the abstract in: http://www.abstractsonline.com/Plan/ViewAbstract.aspx?sKey=723bcad0-3faa-4500-88f6-f25fc9a16aec&cKey=4d9b71ed-f96d-4b2a-9696-1d611a2e0c72&mKey=%7b70007181-01C9-4DE9-A0A2-EEBFA14CD9F1%7d-
dc.description.abstractPURPOSE. Retinal ischemia/reperfusion (I/R) injury is a feature of ocular pathologies such as amaurosis fugax and acute angle-closure glaucoma, leading to irreversible neuronal damage and visual impairment. Our previous studies showed that lutein is neuroprotective in retinal I/R injury. Besides being anti-apoptotic and anti-oxidative, lutein is also implicated to be anti-inflammatory. As Müller cell plays a critical role in inflammation in retinal diseases, the effect of lutein on Müller cells was investigated in a mouse retinal I/R injury model and a chemical-induced hypoxia cell culture model. METHODS. Male C57Bl/6N mice were challenged with 2-hour retinal ischemia followed by 22-hour reperfusion by intraluminal blockade of the internal carotid artery that provides blood supply to the eye. Lutein (0.2mg/kg) or vehicle (10% DMSO) was administered by intraperitoneal injection at 1 hour before and 1 hour after reperfusion. Electroretinography (ERG) and GFAP immunoreactivity were examined in retinal sections. On the other hand, in vitro hypoxia was induced in a retinal Müller cell line (rMC-1) with cobalt (II) chloride. Western blotting of IL-1β, Cox-2, TNFα, and NFκB were then performed to assess the effect of lutein administration. RESULTS. With lutein post-treatment, the deterioration in ERG response and the activation of retinal GFAP were minimized in the animal model of retinal I/R injury. In the cell culture model of hypoxia, lutein administration decreased the levels of IL-1β, Cox-2 and nuclear NFκB but not TNFα. CONCLUSIONS. Lutein post-treatment preserved retinal function and reduced Müller cell gliosis after retinal I/R injury. The reduction of inflammatory factor production from Müller cells after lutein administration suggested an anti-inflammatory role of lutein. Together with our previous studies, these results indicate that lutein protects the retina from I/R damage by its anti-oxidative, anti-apoptotic and anti-inflammatory properties, making lutein an attractive therapeutic agent in eye diseases in which acute ischemia is a feature.-
dc.languageengen_US
dc.publisherAmerican Society of Neuroscience.-
dc.relation.ispartofNeuroscience 2012en_US
dc.subjectRetinal Ganglion Cell-
dc.subjectEye-
dc.subjectGlia-
dc.titleLutein preserved retinal function and minimized inflammatory response in retinal ischemia/reperfusion injuryen_US
dc.typeConference_Paperen_US
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_US
dc.identifier.emailLi, SY: sukyeeli@hku.hken_US
dc.identifier.emailFung, KCF: frederic@hkucc.hku.hken_US
dc.identifier.emailWong, DSH: shdwong@hku.hken_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.identifier.authorityWong, DSH=rp00516en_US
dc.identifier.hkuros223871en_US
dc.publisher.placeUnited States-

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