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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2005-7-13
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pubmed:abstractText |
The accumulation of damage caused by oxidative stress exacerbates cell death in many neurodegenerative diseases. We evaluated the mechanism of neuronal cell death raised by glutamate-induced toxicity, using the immortalized mouse hippocampal cell line HT-22. Our results showed that vitamin E prevented glutamate-induced cell death, accompanied by the decline of cyclooxygenase-2 expression confirmed by reverse transcriptase polymerase chain reaction and immunocytochemistry. Moreover, the neuroprotection was still effective even when vitamin E was supplied after glutamate treatment. The decline of cyclooxygenase-2 activity was also highly correlated with the neural protective effect against glutamate-induced toxicity. These results represent new insights about the timing of vitamin E supplementation after toxic stimulation and one mechanism by which vitamin E could prevent neuronal cell death by controlling cyclooxygenase-2 activity.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/N-(2-cyclohexyloxy-4-nitrophenyl)met...,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrobenzenes,
http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/Vitamin E
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0959-4965
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
16
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1163-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16012341-Animals,
pubmed-meshheading:16012341-Antioxidants,
pubmed-meshheading:16012341-Cell Death,
pubmed-meshheading:16012341-Cell Line,
pubmed-meshheading:16012341-Cyclooxygenase 2,
pubmed-meshheading:16012341-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:16012341-Cyclooxygenase Inhibitors,
pubmed-meshheading:16012341-Dose-Response Relationship, Drug,
pubmed-meshheading:16012341-Drug Interactions,
pubmed-meshheading:16012341-Gene Expression Regulation,
pubmed-meshheading:16012341-Glutamic Acid,
pubmed-meshheading:16012341-Hippocampus,
pubmed-meshheading:16012341-Immunohistochemistry,
pubmed-meshheading:16012341-Mice,
pubmed-meshheading:16012341-Neurons,
pubmed-meshheading:16012341-Nitrobenzenes,
pubmed-meshheading:16012341-Prostaglandin-Endoperoxide Synthases,
pubmed-meshheading:16012341-RNA, Messenger,
pubmed-meshheading:16012341-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:16012341-Sulfonamides,
pubmed-meshheading:16012341-Time Factors,
pubmed-meshheading:16012341-Vitamin E
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pubmed:year |
2005
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pubmed:articleTitle |
Vitamin E prevents the neuronal cell death by repressing cyclooxygenase-2 activity.
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pubmed:affiliation |
Division of Neurobiology and Behavior, Atomic Bomb Disease Institute, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan. kazuyuki@net.nagasaki-u.ac.jp
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pubmed:publicationType |
Journal Article,
Comparative Study
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