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Article: Lutein enhances survival and reduces neuronal damage in a mouse model of ischemic stroke
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TitleLutein enhances survival and reduces neuronal damage in a mouse model of ischemic stroke
 
AuthorsLi, SY1
Yang, D1
Fu, ZJ1
Woo, T1
Wong, D1 1 2
Lo, ACY1 1
 
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
 
CitationNeurobiology Of Disease, 2012, v. 45 n. 1, p. 624-632 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.nbd.2011.10.008
 
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..
 
ISSN0969-9961
2012 Impact Factor: 5.624
2012 SCImago Journal Rankings: 2.334
 
DOIhttp://dx.doi.org/10.1016/j.nbd.2011.10.008
 
ISI Accession Number IDWOS:000297883500069
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLi, SY
 
dc.contributor.authorYang, D
 
dc.contributor.authorFu, ZJ
 
dc.contributor.authorWoo, T
 
dc.contributor.authorWong, D
 
dc.contributor.authorLo, ACY
 
dc.date.accessioned2012-04-10T01:50:11Z
 
dc.date.available2012-04-10T01:50:11Z
 
dc.date.issued2012
 
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..
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationNeurobiology Of Disease, 2012, v. 45 n. 1, p. 624-632 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.nbd.2011.10.008
 
dc.identifier.citeulike9932106
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.nbd.2011.10.008
 
dc.identifier.epage632
 
dc.identifier.hkuros205718
 
dc.identifier.isiWOS:000297883500069
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.

 
dc.identifier.issn0969-9961
2012 Impact Factor: 5.624
2012 SCImago Journal Rankings: 2.334
 
dc.identifier.issue1
 
dc.identifier.pmid22024715
 
dc.identifier.scopuseid_2-s2.0-81955167409
 
dc.identifier.spage624
 
dc.identifier.urihttp://hdl.handle.net/10722/146317
 
dc.identifier.volume45
 
dc.languageeng
 
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ynbdi
 
dc.publisher.placeUnited States
 
dc.relation.ispartofNeurobiology of Disease
 
dc.relation.referencesReferences in Scopus
 
dc.subjectApoptosis
 
dc.subjectCerebral infarct
 
dc.subjectInflammation
 
dc.subjectIschemic stroke
 
dc.subjectOxidative stress
 
dc.subjectXanthophylls
 
dc.titleLutein enhances survival and reduces neuronal damage in a mouse model of ischemic stroke
 
dc.typeArticle
 
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<contributor.author>Wong, D</contributor.author>
<contributor.author>Lo, ACY</contributor.author>
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<description.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 NF&#954;B in the lutein-treated brains. Western blotting data showed decreased levels of Cox-2, pERK, and pI&#954;B, 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. &#169; 2011 Elsevier Inc..</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. null