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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?
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..
Persistent Identifierhttp://hdl.handle.net/10722/146317
ISSN
2015 Impact Factor: 4.856
2015 SCImago Journal Rankings: 2.875
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

 

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.pmid22024715-
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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