Linked Life Data

16934418

Source:http://linkedlifedata.com/resource/pubmed/id/16934418

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-12-25
pubmed:abstractText
Gastrodia elata (Orchidaceae) is a Chinese herb. Our previous study showed that Gastrodia elata is able to reduce epileptic seizures, oxygen free radicals, microglia activation, and apoptosis in kainic acid (KA)-treated rats. Activator protein 1 (AP-1) is involved in modulating the neuronal plasticity and apoptosis. Therefore, the aim of this study was to investigate the role of AP-1 in antiepileptic effect of Gastrodia elata. Gastrodia elata (0.5, 1.0g/kg) or valproic acid (VA, 250mg/kg) was administered orally in Sprague-Dawley rats for 1 week before and 2 weeks after intraperitoneal injection of KA. Protein levels of AP-1 were determined by measuring c-Jun and c-Fos proteins, and the mitogen-activated protein (MAP) kinases activations were determined by measuring the phosphorylations of extracellular signal-regulated kinases, p38, and c-Jun N-terminal kinases (JNKs) in the frontal cortex and the hippocampus of rat brain using Western blotting. These results indicated that pre-treatment with Gastrodia elata or VA activated JNK signal pathway and c-Jun expression, while post-treatment with Gastrodia elata or VA suppressed both the JNK signaling pathway and the c-Jun expression induced by KA. These findings suggested that Gastrodia elata regulated the AP-1 expression via the JNK signaling pathway in KA-induced epilepsy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0378-8741
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
109
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
241-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Gastrodia elata modulated activator protein 1 via c-Jun N-terminal kinase signaling pathway in kainic acid-induced epilepsy in rats.
pubmed:affiliation
Department of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't