Source:http://linkedlifedata.com/resource/pubmed/id/17178414
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2007-2-12
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pubmed:abstractText |
Retinal ischemia is a common cause of visual impairment for humans and animals. Herein, the neuroprotective effects of phenylbutyrate (PBA) upon retinal ischemic injury were investigated using a rat model. Retinal ganglion cells (RGCs) were retrograde labeled with the fluorescent tracer fluorogold (FG) applied to the superior collicoli of test Sprague-Dawley rats. High intraocular pressure and retinal ischemia were induced seven days subsequent to such FG labeling. A dose of either 100 or 400 mg/kg PBA was administered intraperitoneally to test rats at two time points, namely 30 min prior to the induction of retinal ischemia and 1 h subsequent to the cessation of the procedure inducing retinal ischemia. The test-rat retinas were collected seven days subsequent to the induction of retinal ischemia, and densities of surviving RGCs were estimated by counting FG-labeled RGCs within the retina. Histological analysis revealed that ischemic injury caused the loss of retinal RGCs and a net decrease in retinal thickness. For PBA-treated groups, almost 100% of the RGCs were preserved by a pre-ischemia treatment with PBA (at a dose of either 100 or 400 mg/kg), while post-ischemia treatment of RGCs with PBA did not lead to the preservation of RGCs from ischemic injury by PBA as determined by the counting of whole-mount retinas. Pre-ischemia treatment of RGCs with PBA (at a dose of either 100 or 400 mg/kg) significantly reduced the level of ischemia-associated loss of thickness of the total retina, especially the inner retina, and the inner plexiform layer of retina. Besides, PBA treatment significantly reduced the ischemia-induced loss of cells in the ganglion-cell layer of the retina. Taken together, these results suggest that PBA demonstrates a marked neuroprotective effect upon high intraocular pressure-induced retinal ischemia when the PBA is administered prior to ischemia induction.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0014-4835
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
84
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
486-92
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pubmed:meshHeading |
pubmed-meshheading:17178414-Animals,
pubmed-meshheading:17178414-Cell Count,
pubmed-meshheading:17178414-Cell Death,
pubmed-meshheading:17178414-Dose-Response Relationship, Drug,
pubmed-meshheading:17178414-Glaucoma,
pubmed-meshheading:17178414-Ischemia,
pubmed-meshheading:17178414-Male,
pubmed-meshheading:17178414-Microscopy, Fluorescence,
pubmed-meshheading:17178414-Models, Animal,
pubmed-meshheading:17178414-Phenylbutyrates,
pubmed-meshheading:17178414-Rats,
pubmed-meshheading:17178414-Rats, Sprague-Dawley,
pubmed-meshheading:17178414-Reperfusion Injury,
pubmed-meshheading:17178414-Retinal Diseases,
pubmed-meshheading:17178414-Retinal Ganglion Cells,
pubmed-meshheading:17178414-Retinal Vessels
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pubmed:year |
2007
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pubmed:articleTitle |
Retinal ischemic injury rescued by sodium 4-phenylbutyrate in a rat model.
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pubmed:affiliation |
Graduate Institute of Veterinary Medicine, College of Bio-resources and Agriculture, National Taiwan University, Taipei, Taiwan.
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pubmed:publicationType |
Journal Article
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