Source:http://linkedlifedata.com/resource/pubmed/id/21424281
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-4-21
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pubmed:abstractText |
Caffeoylquinic acid (CQA) is one of the phenylpropanoids found in a variety of natural resources and foods, such as sweet potatoes, propolis, and coffee. Previously, we reported that 3,5-di-O-caffeoylquinic acid (3,5-di-CQA) has a neuroprotective effect against amyloid-? (A?)-induced cell death through the overexpression of glycolytic enzyme. Additionally, 3,5-di-CQA administration induced the improvement of spatial learning and memory on senescence accelerated-prone mice (SAMP8). The aim of this study was to investigate whether 3,4,5-tri-O-caffeoylquinic acid (3,4,5-tri-CQA), isolated from propolis, shows a neuroprotective effect against A?-induced cell death on human neuroblastoma SH-SY5Y cells. To clarify the possible mechanism, we performed proteomics and real-time RT-PCR as well as a measurement of the intracellular adenosine triphosphate (ATP) level. These results showed that 3,4,5-tri-CQA attenuated the cytotoxicity and prevented A?-mediated apoptosis. Glycolytic enzymes, phosphoglycerate mutase 1 (PGAM1) and glyceraldehyde-3-phosphate dehydrogenase (G3PDH) were overexpressed in co-treated cells with both 3,4,5-tri-CQA and A?. The mRNA expression of PGAM1, G3PDH, and phosphoglycerate kinase 1 (PGK1), and intracellular ATP level were also increased in 3,4,5-tri-CQA treated cells. Taken together the findings in our study suggests that 3,4,5-tri-CQA shows a neuroprotective effect against A?-induced cell death through the upregulation of glycolytic enzyme mRNA as well as ATP production activation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:status |
PubMed-not-MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0920-9069
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
63
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
191-200
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pubmed:year |
2011
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pubmed:articleTitle |
3,4,5-tri-O-caffeoylquinic acid inhibits amyloid ?-mediated cellular toxicity on SH-SY5Y cells through the upregulation of PGAM1 and G3PDH.
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pubmed:affiliation |
Graduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8572, Japan.
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pubmed:publicationType |
Journal Article
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