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Article: Anti-inflammatory effects of lutein in retinal ischemic/ hypoxic injury: In vivo and in vitro studies

TitleAnti-inflammatory effects of lutein in retinal ischemic/ hypoxic injury: In vivo and in vitro studies
Authors
Issue Date2012
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, 2012, v. 53 n. 10, p. 5976-5984 How to Cite?
AbstractPURPOSE: Lutein protects retinal neurons by its anti-oxidative and anti-apoptotic properties in ischemia/reperfusion (I/R) injury while its anti-inflammatory effects remain unknown. As Müller cells play a critical role in retinal inflammation, the effect of lutein on Müller cells was investigated in a murine model of I/R injury and a culture model of hypoxic damage. METHODS: Unilateral retinal I/R was induced by a blockade of internal carotid artery using the intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein (0.2 mg/kg) or vehicle was administered. Flash electroretinogram (flash ERG) and glial fibrillary acidic protein (GFAP) activation were assessed. Lutein's effect on Müller cells was further evaluated in immortalized rat Müller cells (rMC-1) challenged with cobalt chloride-induced hypoxia. Levels of IL-1β, cyclooxygenase-2 (Cox-2), TNFoα and nuclear factor-NF-kappa-B (NF-κB) were examined by Western blot analysis. RESULTS: Lutein treatment minimized deterioration of b-wave/a-wave ratio and oscillatory potentials as well as inhibited upregulation of GFAP in retinal I/R injury. In cultured Müller cells, lutein treatment increased cell viability and reduced level of nuclear NF-κB, IL-1β, and Cox-2, but not TNFα after hypoxic injury. CONCLUSIONS: Reduced gliosis in I/R retina was observed with lutein treatment, which may contribute to preserved retinal function. Less production of pro-inflammatory factors from Müller cells suggested an anti-inflammatory role of lutein in retinal ischemic/hypoxic injury. Together with our previous studies, our results suggest that lutein protected the retina from ischemic/hypoxic damage by its anti-oxidative, antiapoptotic, and anti-inflammatory properties.
Persistent Identifierhttp://hdl.handle.net/10722/176490
ISSN
2015 Impact Factor: 3.427
2015 SCImago Journal Rankings: 2.008
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, SYen_US
dc.contributor.authorFung, FKCen_US
dc.contributor.authorFu, ZJen_US
dc.contributor.authorWong, Den_US
dc.contributor.authorChan, HHLen_US
dc.contributor.authorLo, ACYen_US
dc.date.accessioned2012-11-26T09:11:45Z-
dc.date.available2012-11-26T09:11:45Z-
dc.date.issued2012en_US
dc.identifier.citationInvestigative Ophthalmology And Visual Science, 2012, v. 53 n. 10, p. 5976-5984en_US
dc.identifier.issn0146-0404en_US
dc.identifier.urihttp://hdl.handle.net/10722/176490-
dc.description.abstractPURPOSE: Lutein protects retinal neurons by its anti-oxidative and anti-apoptotic properties in ischemia/reperfusion (I/R) injury while its anti-inflammatory effects remain unknown. As Müller cells play a critical role in retinal inflammation, the effect of lutein on Müller cells was investigated in a murine model of I/R injury and a culture model of hypoxic damage. METHODS: Unilateral retinal I/R was induced by a blockade of internal carotid artery using the intraluminal method in mice. Ischemia was maintained for 2 hours followed by 22 hours of reperfusion, during which either lutein (0.2 mg/kg) or vehicle was administered. Flash electroretinogram (flash ERG) and glial fibrillary acidic protein (GFAP) activation were assessed. Lutein's effect on Müller cells was further evaluated in immortalized rat Müller cells (rMC-1) challenged with cobalt chloride-induced hypoxia. Levels of IL-1β, cyclooxygenase-2 (Cox-2), TNFoα and nuclear factor-NF-kappa-B (NF-κB) were examined by Western blot analysis. RESULTS: Lutein treatment minimized deterioration of b-wave/a-wave ratio and oscillatory potentials as well as inhibited upregulation of GFAP in retinal I/R injury. In cultured Müller cells, lutein treatment increased cell viability and reduced level of nuclear NF-κB, IL-1β, and Cox-2, but not TNFα after hypoxic injury. CONCLUSIONS: Reduced gliosis in I/R retina was observed with lutein treatment, which may contribute to preserved retinal function. Less production of pro-inflammatory factors from Müller cells suggested an anti-inflammatory role of lutein in retinal ischemic/hypoxic injury. Together with our previous studies, our results suggest that lutein protected the retina from ischemic/hypoxic damage by its anti-oxidative, antiapoptotic, and anti-inflammatory properties.en_US
dc.languageengen_US
dc.publisherAssociation for Research in Vision and Ophthalmology. The Journal's web site is located at http://www.iovs.orgen_US
dc.relation.ispartofInvestigative Ophthalmology and Visual Scienceen_US
dc.titleAnti-inflammatory effects of lutein in retinal ischemic/ hypoxic injury: In vivo and in vitro studiesen_US
dc.typeArticleen_US
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_US
dc.identifier.authorityLo, ACY=rp00425en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1167/iovs.12-10007en_US
dc.identifier.pmid22871829-
dc.identifier.scopuseid_2-s2.0-84866067679en_US
dc.identifier.hkuros223811-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84866067679&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume53en_US
dc.identifier.issue10en_US
dc.identifier.spage5976en_US
dc.identifier.epage5984en_US
dc.identifier.isiWOS:000309526200001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLo, ACY=7102780640en_US
dc.identifier.scopusauthoridLi, SY=24329630700en_US
dc.identifier.scopusauthoridFung, FKC=55355611500en_US
dc.identifier.scopusauthoridFu, ZJ=36908915500en_US
dc.identifier.scopusauthoridWong, D=55323014200en_US
dc.identifier.scopusauthoridChan, HHL=55017439000en_US
dc.customcontrol.immutablejt 130917-

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