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Article: Lutein enhances survival and reduces neuronal damage in a mouse model of ischemic stroke

TitleLutein enhances survival and reduces neuronal damage in a mouse model of ischemic stroke
Authors
KeywordsApoptosis
Cerebral infarct
Inflammation
Ischemic stroke
Oxidative stress
Xanthophylls
Issue Date2012
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdi
Citation
Neurobiology Of Disease, 2012, v. 45 n. 1, p. 624-632 How to Cite?
Abstract
Introduction: Stroke is one of the leading causes of death worldwide. Protective agents that could diminish the injuries induced by cerebral ischemia/reperfusion (I/R) are crucial to alleviate the detrimental outcome of stroke. The aim of this study is to investigate the protective roles of lutein in cerebral I/R injury. Methods: Two-hour cerebral ischemia was induced by unilateral middle cerebral artery occlusion (MCAo) in mice. Either lutein (0.2. mg/kg) or vehicle was given to mice intraperitoneally 1. h after MCAo and 1. h after reperfusion. Neurological deficits were evaluated at 22. h after reperfusion while survival rate was assessed daily until 7. days after reperfusion. Brains were cut into 2. mm-thick coronal slices and stained with 2% 2,3,5-triphenyltetrazolium chloride to determine the infarct size after MCAo. Paraffin-embedded brain sections were prepared for TUNEL assay and immunohistochemistry. Protein lysate was collected for Western blotting experiments. Results: Higher survival rate, better neurological scores, smaller infarct area and smaller infarct volume were noted in the lutein-treated group. Immunohistochemistry data showed a decrease of immunoreactivity of nitrotyrosine, poly(ADP-ribose) and NFκB in the lutein-treated brains. Western blotting data showed decreased levels of Cox-2, pERK, and pIκB, but increased levels of Bcl-2, heat shock protein 70 and pAkt in the lutein-treated brains. Conclusions: Post-treatment of lutein protected the brain from I/R injury, probably by its anti-apoptotic, anti-oxidative and anti-inflammatory properties. These suggest that lutein could diminish the deleterious outcomes of cerebral I/R and may be used as a potential treatment for stroke patients. © 2011 Elsevier Inc..
Persistent Identifierhttp://hdl.handle.net/10722/146317
ISSN
2013 Impact Factor: 5.202
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilHKU773210M
University of Hong Kong
Funding Information:

This research was supported by the grants from the Hong Kong Research Grants Council (GRF #HKU773210M) and the University Development Fund from The University of Hong Kong.

References

 

Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. null
DC FieldValueLanguage
dc.contributor.authorLi, SYen_HK
dc.contributor.authorYang, Den_HK
dc.contributor.authorFu, ZJen_HK
dc.contributor.authorWoo, Ten_HK
dc.contributor.authorWong, Den_HK
dc.contributor.authorLo, ACYen_HK
dc.date.accessioned2012-04-10T01:50:11Z-
dc.date.available2012-04-10T01:50:11Z-
dc.date.issued2012en_HK
dc.identifier.citationNeurobiology Of Disease, 2012, v. 45 n. 1, p. 624-632en_HK
dc.identifier.issn0969-9961en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146317-
dc.description.abstractIntroduction: Stroke is one of the leading causes of death worldwide. Protective agents that could diminish the injuries induced by cerebral ischemia/reperfusion (I/R) are crucial to alleviate the detrimental outcome of stroke. The aim of this study is to investigate the protective roles of lutein in cerebral I/R injury. Methods: Two-hour cerebral ischemia was induced by unilateral middle cerebral artery occlusion (MCAo) in mice. Either lutein (0.2. mg/kg) or vehicle was given to mice intraperitoneally 1. h after MCAo and 1. h after reperfusion. Neurological deficits were evaluated at 22. h after reperfusion while survival rate was assessed daily until 7. days after reperfusion. Brains were cut into 2. mm-thick coronal slices and stained with 2% 2,3,5-triphenyltetrazolium chloride to determine the infarct size after MCAo. Paraffin-embedded brain sections were prepared for TUNEL assay and immunohistochemistry. Protein lysate was collected for Western blotting experiments. Results: Higher survival rate, better neurological scores, smaller infarct area and smaller infarct volume were noted in the lutein-treated group. Immunohistochemistry data showed a decrease of immunoreactivity of nitrotyrosine, poly(ADP-ribose) and NFκB in the lutein-treated brains. Western blotting data showed decreased levels of Cox-2, pERK, and pIκB, but increased levels of Bcl-2, heat shock protein 70 and pAkt in the lutein-treated brains. Conclusions: Post-treatment of lutein protected the brain from I/R injury, probably by its anti-apoptotic, anti-oxidative and anti-inflammatory properties. These suggest that lutein could diminish the deleterious outcomes of cerebral I/R and may be used as a potential treatment for stroke patients. © 2011 Elsevier Inc..en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdien_HK
dc.relation.ispartofNeurobiology of Diseaseen_HK
dc.subjectApoptosisen_HK
dc.subjectCerebral infarcten_HK
dc.subjectInflammationen_HK
dc.subjectIschemic strokeen_HK
dc.subjectOxidative stressen_HK
dc.subjectXanthophyllsen_HK
dc.titleLutein enhances survival and reduces neuronal damage in a mouse model of ischemic strokeen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, D: shdwong@hku.hken_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.authorityWong, D=rp00516en_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.nbd.2011.10.008en_HK
dc.identifier.pmid22024715en_HK
dc.identifier.scopuseid_2-s2.0-81955167409en_HK
dc.identifier.hkuros205718-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-81955167409&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue1en_HK
dc.identifier.spage624en_HK
dc.identifier.epage632en_HK
dc.identifier.isiWOS:000297883500069-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, SY=24329630700en_HK
dc.identifier.scopusauthoridYang, D=37662476600en_HK
dc.identifier.scopusauthoridFu, ZJ=36908915500en_HK
dc.identifier.scopusauthoridWoo, T=53265281800en_HK
dc.identifier.scopusauthoridWong, D=7401536078en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.citeulike9932106-

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