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Conference Paper: Neuroprotective effects of lutein on inner retinal neurons in a model of acute retinal ischemia/reperfusion

TitleNeuroprotective effects of lutein on inner retinal neurons in a model of acute retinal ischemia/reperfusion
Authors
Issue Date2008
PublisherSociety for Neuroscience
Citation
Neuroscience 2008, Washington, DC, 15-19 November 2008, Program#/Poster#: 652.7/BB15 How to Cite?
AbstractRetinal ischemia/reperfusion (I/R) is common in many ocular diseases, and leads to irreversible neuronal cell and structural damage. It is well known that lutein, one of the potent antioxidants, protects retina in age-related macular degeneration (AMD). However, the neuroprotective effect of lutein on retinal I/R is not yet explored. In the present study, acute unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Here, 2 hrs of ischemia was induced followed by 22 hrs of reperfusion. At 1 hr before and 1 hr after the onset of reperfusion either lutein or vehicle was administrated by intraperitoneal injection. Our findings showed that severe neuronal cell loss in retinal ganglion cells (RGCs) and inner retinal swelling was observed in retina after I/R insult. Ischemia also caused deleterious effect on other inner retinal neurons, including amacrine cells, bipolar cells and horizontal cells. In addition, expression levels of two oxidative stress markers, nitrotyrosine and poly(ADP-ribose), were elevated in ischemic retina. However, lutein administration protected RGCs as well as other inner retinal cells. Besides, retinal swelling induced by I/R was reduced after lutein treatment. Oxidative stress was obviously decreased in lutein-treated retina. Result herein demonstrated that lutein rescued the retina from I/R insult. Moreover, lutein improved the neurological behavior and decreased the death rate, indicating that lutein may exert important neuroprotective effects on tissues other than on retina alone. This study provides more information on the neuroprotection of retinal neurons by lutein after acute retinal I/R injury. Most importantly, our study is the first to show that lutein is beneficial to inner retinal neurons. In addition, the current study provides more insights on broadening the use of lutein to prevent or retard the progression of retinal pathologies other than AMD in the future.
Persistent Identifierhttp://hdl.handle.net/10722/61454

 

DC FieldValueLanguage
dc.contributor.authorLi, SYen_HK
dc.contributor.authorFu, Zen_HK
dc.contributor.authorMa, Hen_HK
dc.contributor.authorJang, WCen_HK
dc.contributor.authorWong, DSHen_HK
dc.contributor.authorLo, ACYen_HK
dc.date.accessioned2010-07-13T03:40:00Z-
dc.date.available2010-07-13T03:40:00Z-
dc.date.issued2008en_HK
dc.identifier.citationNeuroscience 2008, Washington, DC, 15-19 November 2008, Program#/Poster#: 652.7/BB15-
dc.identifier.urihttp://hdl.handle.net/10722/61454-
dc.description.abstractRetinal ischemia/reperfusion (I/R) is common in many ocular diseases, and leads to irreversible neuronal cell and structural damage. It is well known that lutein, one of the potent antioxidants, protects retina in age-related macular degeneration (AMD). However, the neuroprotective effect of lutein on retinal I/R is not yet explored. In the present study, acute unilateral retinal I/R was induced by the blockade of internal carotid artery using intraluminal method in mice. Here, 2 hrs of ischemia was induced followed by 22 hrs of reperfusion. At 1 hr before and 1 hr after the onset of reperfusion either lutein or vehicle was administrated by intraperitoneal injection. Our findings showed that severe neuronal cell loss in retinal ganglion cells (RGCs) and inner retinal swelling was observed in retina after I/R insult. Ischemia also caused deleterious effect on other inner retinal neurons, including amacrine cells, bipolar cells and horizontal cells. In addition, expression levels of two oxidative stress markers, nitrotyrosine and poly(ADP-ribose), were elevated in ischemic retina. However, lutein administration protected RGCs as well as other inner retinal cells. Besides, retinal swelling induced by I/R was reduced after lutein treatment. Oxidative stress was obviously decreased in lutein-treated retina. Result herein demonstrated that lutein rescued the retina from I/R insult. Moreover, lutein improved the neurological behavior and decreased the death rate, indicating that lutein may exert important neuroprotective effects on tissues other than on retina alone. This study provides more information on the neuroprotection of retinal neurons by lutein after acute retinal I/R injury. Most importantly, our study is the first to show that lutein is beneficial to inner retinal neurons. In addition, the current study provides more insights on broadening the use of lutein to prevent or retard the progression of retinal pathologies other than AMD in the future.-
dc.languageengen_HK
dc.publisherSociety for Neuroscience-
dc.relation.ispartofSociety for Neuroscience Annual Meeting-
dc.titleNeuroprotective effects of lutein on inner retinal neurons in a model of acute retinal ischemia/reperfusionen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLi, SY: rachelli@hkusua.hku.hken_HK
dc.identifier.emailWong, DSH: shdwong@hku.hken_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.authorityWong, DSH=rp00516en_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.hkuros154565en_HK

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