Linked Life Data

19012619

Source:http://linkedlifedata.com/resource/pubmed/id/19012619

Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:19012619rdf:typepubmed:Citationlld:pubmed
pubmed-article:19012619lifeskim:mentionsumls-concept:C0001480lld:lifeskim
pubmed-article:19012619lifeskim:mentionsumls-concept:C0439799lld:lifeskim
pubmed-article:19012619lifeskim:mentionsumls-concept:C1882151lld:lifeskim
pubmed-article:19012619pubmed:issue5Alld:pubmed
pubmed-article:19012619pubmed:dateCreated2008-11-17lld:pubmed
pubmed-article:19012619pubmed:abstractTextAs activated microglia (MG) is an early sign that often precedes and triggers neuronal death, inhibition of microglial activation and reduction of subsequent neurotoxicity may offer therapeutic benefit. The present study demonstrates that rat primary cultured MG expressed Kir6.1 and SUR2 subunits of K(ATP) channel, which was identical to that expressed in BV-2 microglial cell line. The classic K(ATP) channel opener pinacidil and selective mitochondrial K(ATP) (mito-K(ATP)) channel opener diazoxide prevented rotenone-induced microglial activation and production of pro-inflammatory factors (tumour necrosis factor[TNF]-alpha and prostaglandin E(2)[PGE(2)]). And the effects of pinacidil and diazoxide were reversed by mito-K(ATP) blocker 5-hydroxydecanoate (5-HD), indicating that mito-K(ATP) channels participate in the regulation of microglial activation. Moreover, the underlying mechanisms involved the stabilization of mitochodrial membrane potential and inhibition of p38/c-Jun-N-terminal kinase (JNK) activation in microglia. Furthermore, the in vivo study confirmed that diazoxide exhibited neuroprotective effects against rotenone along with the inhibition of microglial activation and neuroinflammation. Thus, microglial mito-K(ATP) channel might be a novel prospective target for the treatment of neuroinflammation-related degenerative disorders such as Parkinson's disease.lld:pubmed
pubmed-article:19012619pubmed:languageenglld:pubmed
pubmed-article:19012619pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:citationSubsetIMlld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:19012619pubmed:statusMEDLINElld:pubmed
pubmed-article:19012619pubmed:issn1582-1838lld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:HuGangGlld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:SunTaoTlld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:YaoHong-HongH...lld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:ZhouFangFlld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:DingJian-HuaJ...lld:pubmed
pubmed-article:19012619pubmed:authorpubmed-author:WuJia-YongJYlld:pubmed
pubmed-article:19012619pubmed:issnTypePrintlld:pubmed
pubmed-article:19012619pubmed:volume12lld:pubmed
pubmed-article:19012619pubmed:ownerNLMlld:pubmed
pubmed-article:19012619pubmed:authorsCompleteYlld:pubmed
pubmed-article:19012619pubmed:pagination1559-70lld:pubmed
pubmed-article:19012619pubmed:dateRevised2009-11-19lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:meshHeadingpubmed-meshheading:19012619...lld:pubmed
pubmed-article:19012619pubmed:articleTitleOpening of microglial K(ATP) channels inhibits rotenone-induced neuroinflammation.lld:pubmed
pubmed-article:19012619pubmed:affiliationJiangsu Key Laboratory of Neurodegeneration, Department of Anatomy Histology, Pharmacology Nanjing Medical University Nanjing, Jiangsu, P. R. China.lld:pubmed
pubmed-article:19012619pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:19012619pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:19012619lld:pubmed