Linked Life Data

18946795

Source:http://linkedlifedata.com/resource/pubmed/id/18946795

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2008-11-5
pubmed:abstractText
This study investigated the effects of (-)-epicatechin (EC), its oligomers, dimer B2 (B2) and trimer C1 (C1), on calcium-dependent cell oxidation. Jurkat T cells were subjected to a Ca(2+) mobilization challenge by replacing Na(+) with K(+) in the incubation media. A 249+/-38% increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) was observed and that effect was prevented by the presence of inhibitors of Ca(2+) mobilization and entrance. The pre-incubation of the cells in the presence of EC, B2 or C1 prevented K(+)-mediated increase in [Ca(2+)](i). IC(50) were 10, 24 and 196 nMfor EC, B2 and C1, respectively. Cell membrane depolarization was affected by K(+), but neither inhibitors of Ca(2+) mobilization nor EC, B2 or C1 modified the increase in membrane potential. An 84+/-7% increase in cell oxidants was observed after cell exposure to K(+). This increase was prevented by the inhibition of Ca(2+) mobilization, NADPH oxidase and protein kinase C, as well as by 10 nM EC, 10 nM B2 or 100 nM C1. In addition, EC and B2 (100 nM) significantly inhibited the activation of the [Ca(2+)](i)-regulated transcription factor NFAT. These results indicate that EC and related oligomers, assayed at physiologically achievable concentrations, can modulate [Ca(2+)](i) and then prevent cell oxidation and other Ca(2+)-regulated events.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1029-2470
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
42
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
864-72
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
(-)-Epicatechin and related procyanidins modulate intracellular calcium and prevent oxidation in Jurkat T cells.
pubmed:affiliation
Department of Biological Chemistry, IQUIFIB-CONICET, School of Pharmacy and Biochemistry, University of Buenos Aires, Argentina.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't