Linked Life Data

14718588

Source:http://linkedlifedata.com/resource/pubmed/id/14718588

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-3-29
pubmed:abstractText
The retinal ischemic-reperfusion stress (130 mm Hg, 45 min) caused neuronal damage throughout all cell layers and reduced the thickness of retinal layer by 30% at 7 days after the stress of mouse retina. The intravitreous injection of 100 pmol of nefiracetam, a cognition-enhancer, completely prevented the damage when it was given 30 min before and 3 h after the stress. Partial prevention was observed when it was given 24 h after the stress, or low dose (10 pmol) nefiracetam was given 30 min before the stress. However, aniracetam had no effect. In the retinal cell line N18-RE-105, the ischemic-reperfusion stress by 2 h culture under the serum-free condition with low oxygen (less of 0.4% O(2)) and low glucose (1 mM) caused necrosis or apoptosis in the low-density (0.5 x 10(4) cell/cm(2))or high-density (5 x 10(4) cell/cm(2)) culture, respectively. The necrosis showed membrane disruption, loss of electron density, and mitochondrial swelling, whereas apoptosis showed nuclear fragmentation and condensation in transmission electron microscopical analyses and in experiments using specific cell death markers. Nefiracetam inhibited both necrosis and apoptosis, whereas brain-derived neurotrophic factor (BDNF) inhibited only apoptosis. The cell-protective actions of nefiracetam were abolished by nifedipine and omega-conotoxin GVIA, L-type and N-type calcium channel blocker, but not by PD98059 or wortmannin, extracellular signal-regulated kinase 1/2 or phosphoinositide 3-kinase inhibitor, respectively, whereas those of BDNF were abolished by PD98059 and wortmannin, but not by nifedipine and omega-conotoxin GVIA. All these findings suggest that nefiracetam inhibit necrosis and apoptosis occurred in the ischemic/hypoxic neuronal injury through an increase in Ca(2+) influx.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
309
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
200-7
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
The cognition-enhancer nefiracetam inhibits both necrosis and apoptosis in retinal ischemic models in vitro and in vivo.
pubmed:affiliation
Division of Molecular Pharmacology and Neuroscience, Nagasaki University Graduate School of Biomedical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan. ueda@net.nagasaki-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't