Linked Life Data

16952351

Source:http://linkedlifedata.com/resource/pubmed/id/16952351

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:16952351rdf:typepubmed:Citationlld:pubmed
pubmed-article:16952351lifeskim:mentionsumls-concept:C0027882lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0521447lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0061751lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0021467lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0332281lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C1521761lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0021469lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0205225lld:lifeskim
pubmed-article:16952351lifeskim:mentionsumls-concept:C0815279lld:lifeskim
pubmed-article:16952351pubmed:issue1-3lld:pubmed
pubmed-article:16952351pubmed:dateCreated2006-9-19lld:pubmed
pubmed-article:16952351pubmed:abstractTextGlycyrrhizic acid is an herbal drug with a broad spectrum of antiviral activities and pharmacological effects and multiple sites of action. We investigated whether glycyrrhizic acid protects against glutamate-induced excitotoxicity and the underlying mechanisms. We found that glycyrrhizic acid protected against neurotoxicity in rat primary neuronal cultures and hippocampal slices by suppression of the glutamate-induced apoptosis. Glycyrrhizic acid conferred neuroprotective properties in a concentration-dependent manner, as determined by cell survival, apoptosis, and Ca(2+) influx. Glycyrrhizic acid selectively inhibited the Ca(2+) influx activated through N-methyl-D-aspartate (NMDA) receptor by glutamate, but not through membrane depolarization elicited by high K(+) induction. Glycyrrhizic acid treatment also diminished glutamate-induced DNA fragmentation and cleavage of poly (ADP-ribose) polymerase (PARP). Electrophoretic mobility shift assay (EMSA) indicated that glycyrrhizic acid inhibited the binding activity of nuclear factor kappaB (NF-kappaB) to its target elements. Western blot analysis of NF-kappaB inhibitor (IkappaBalpha) protein revealed that the inhibitory effect of glycyrrhizic acid on glutamate-induced activation of NF-kappaB activity was attributable to the inhibition of IkappaB kinase activity. Thus, the site of action of glycyrrhizic acid could be a downstream consequence of Ca(2+)entry through NMDA receptors and that NF-kappaB may be one downstream target in this process. These observations suggest that glycyrrhizic acid may be of therapeutic value for the prevention of cerebral damage elicited by the glutamate.lld:pubmed
pubmed-article:16952351pubmed:languageenglld:pubmed
pubmed-article:16952351pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:citationSubsetIMlld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:16952351pubmed:statusMEDLINElld:pubmed
pubmed-article:16952351pubmed:monthOctlld:pubmed
pubmed-article:16952351pubmed:issn0014-2999lld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:ChanMing-Huan...lld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:LinJung-Chung...lld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:LinYi-RuuYRlld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:CherngJaw-Min...lld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:LinHsiang-JuH...lld:pubmed
pubmed-article:16952351pubmed:authorpubmed-author:HungMan-ShanM...lld:pubmed
pubmed-article:16952351pubmed:issnTypePrintlld:pubmed
pubmed-article:16952351pubmed:day10lld:pubmed
pubmed-article:16952351pubmed:volume547lld:pubmed
pubmed-article:16952351pubmed:ownerNLMlld:pubmed
pubmed-article:16952351pubmed:authorsCompleteYlld:pubmed
pubmed-article:16952351pubmed:pagination10-21lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:meshHeadingpubmed-meshheading:16952351...lld:pubmed
pubmed-article:16952351pubmed:year2006lld:pubmed
pubmed-article:16952351pubmed:articleTitleInhibition of nuclear factor kappaB is associated with neuroprotective effects of glycyrrhizic acid on glutamate-induced excitotoxicity in primary neurons.lld:pubmed
pubmed-article:16952351pubmed:affiliationDepartment of Internal Medicine, E-Da Hospital, I-Shou University, Kaohsiung, Taiwan, ROC.lld:pubmed
pubmed-article:16952351pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:16952351pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed