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Conference Paper: Lycium barbarum extracts preserve retinal function and reduce neuronal damage in a mouse model of transient retinal ischemia

TitleLycium barbarum extracts preserve retinal function and reduce neuronal damage in a mouse model of transient retinal ischemia
Authors
Issue Date2013
PublisherAssociation for Research in Vision and Ophthalmology (ARVO)
Citation
The 2013 Annual Meeting of the Association for Research in Vision and Ophthalmology (ARVO), Seattle, WA., 5-9 May 2013. How to Cite?
AbstractPURPOSE: Retinal ischemia is a common feature shared by many blindness-causing eye diseases including retinal vascular occlusion, diabetic retinopathy, glaucoma, and retinopathy of prematurity. Retinal dysfunction and neuronal cell death are complications of ischemic insult. We aim to investigate the neuroprotective effects of Lycium barbarum polysaccharides (LBP), extracts from an anti-aging and anti-oxidation Oriental medicine, on visual function and retinal neurons in a mouse model of transient retinal ischemia. METHODS: Retinal ischemia was induced by intraluminal filamentous occlusion of the internal carotid artery for 2 hours and reperfusion was allowed by filament removal. Either LBP or phosphate-buffered saline was administered daily through a gastric tube for 7 days prior to retinal ischemia as well as 1 day, 3 days and 7 days after reperfusion. Scotopic electroretinography was performed to evaluate visual function. Paraffin-embedded retinal sections were prepared 7 days after reperfusion. Viable cells in the ganglion cell layer were counted and inner retinal thickness was measured. Expression levels of protein kinase C (PKC-α), calretinin, glial fibrillary acidic protein (GFAP) and glutamine synthase were investigated by immunohistochemistry. RESULTS: 2-hour retinal ischemia leads to sustained inhibition of b- wave amplitude and oscillatory potentials (OPs). LBP-treated mice exhibited greater b-wave and OPs responses at 1 day, 3 days and 7 days after reperfusion indicating persistent functional protection of bipolar cells, amacrine cells and Müller cells. In addition, ischemic insult resulted in fewer viable cells and decreased retinal thickness, as well as reduced immunoreactivity of PKC-α, fewer calretinin-positive cells and increased expression of GFAP. These changes were diminished in LBP-treated retina which was in line with the electroretinography findings. CONCLUSIONS: LBP treatment effectively preserved retinal function as well as reduced neuronal death and glial activation. The present study suggests that LBP may serve as a neuroprotective agent in retinal ischemic diseases.
DescriptionTheme: Life-changing Research
Poster Session 338 - Retinal Degeneration and Neuroprotection: Program ID: 3262 - A0053
Persistent Identifierhttp://hdl.handle.net/10722/191080

 

DC FieldValueLanguage
dc.contributor.authorYang, Den_US
dc.contributor.authorMa, Den_US
dc.contributor.authorChang, RCCen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorWong, DSHen_US
dc.contributor.authorLo, AC-
dc.date.accessioned2013-09-17T16:15:40Z-
dc.date.available2013-09-17T16:15:40Z-
dc.date.issued2013en_US
dc.identifier.citationThe 2013 Annual Meeting of the Association for Research in Vision and Ophthalmology (ARVO), Seattle, WA., 5-9 May 2013.en_US
dc.identifier.urihttp://hdl.handle.net/10722/191080-
dc.descriptionTheme: Life-changing Research-
dc.descriptionPoster Session 338 - Retinal Degeneration and Neuroprotection: Program ID: 3262 - A0053-
dc.description.abstractPURPOSE: Retinal ischemia is a common feature shared by many blindness-causing eye diseases including retinal vascular occlusion, diabetic retinopathy, glaucoma, and retinopathy of prematurity. Retinal dysfunction and neuronal cell death are complications of ischemic insult. We aim to investigate the neuroprotective effects of Lycium barbarum polysaccharides (LBP), extracts from an anti-aging and anti-oxidation Oriental medicine, on visual function and retinal neurons in a mouse model of transient retinal ischemia. METHODS: Retinal ischemia was induced by intraluminal filamentous occlusion of the internal carotid artery for 2 hours and reperfusion was allowed by filament removal. Either LBP or phosphate-buffered saline was administered daily through a gastric tube for 7 days prior to retinal ischemia as well as 1 day, 3 days and 7 days after reperfusion. Scotopic electroretinography was performed to evaluate visual function. Paraffin-embedded retinal sections were prepared 7 days after reperfusion. Viable cells in the ganglion cell layer were counted and inner retinal thickness was measured. Expression levels of protein kinase C (PKC-α), calretinin, glial fibrillary acidic protein (GFAP) and glutamine synthase were investigated by immunohistochemistry. RESULTS: 2-hour retinal ischemia leads to sustained inhibition of b- wave amplitude and oscillatory potentials (OPs). LBP-treated mice exhibited greater b-wave and OPs responses at 1 day, 3 days and 7 days after reperfusion indicating persistent functional protection of bipolar cells, amacrine cells and Müller cells. In addition, ischemic insult resulted in fewer viable cells and decreased retinal thickness, as well as reduced immunoreactivity of PKC-α, fewer calretinin-positive cells and increased expression of GFAP. These changes were diminished in LBP-treated retina which was in line with the electroretinography findings. CONCLUSIONS: LBP treatment effectively preserved retinal function as well as reduced neuronal death and glial activation. The present study suggests that LBP may serve as a neuroprotective agent in retinal ischemic diseases.-
dc.languageengen_US
dc.publisherAssociation for Research in Vision and Ophthalmology (ARVO)-
dc.relation.ispartofARVO 2013 Annual Meetingen_US
dc.titleLycium barbarum extracts preserve retinal function and reduce neuronal damage in a mouse model of transient retinal ischemiaen_US
dc.typeConference_Paperen_US
dc.identifier.emailChang, RCC: rccchang@hku.hken_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.identifier.emailWong, DSH: shdwong@hku.hken_US
dc.identifier.emailLo, AC: amylo@hkucc.hku.hken_US
dc.identifier.authorityChang, RCC=rp00470en_US
dc.identifier.authoritySo, KF=rp00329en_US
dc.identifier.authorityWong, DSH=rp00516en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros223813en_US
dc.publisher.placeUnited States-

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