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dc.contributor.authorHenninger, Nils
dc.contributor.authorSicard, Kenneth M.
dc.contributor.authorBouley, James P.
dc.contributor.authorFisher, Marc
dc.contributor.authorStagliano, Nancy E.
dc.date2022-08-11T08:09:27.000
dc.date.accessioned2022-08-23T16:31:22Z
dc.date.available2022-08-23T16:31:22Z
dc.date.issued2006-02-23
dc.date.submitted2008-04-28
dc.identifier.citationNeurosci Lett. 2006 May 8;398(3):300-5. Epub 2006 Feb 21. <a href="http://dx.doi.org/10.1016/j.neulet.2006.01.015">Link to article on publisher's site</a>
dc.identifier.issn0304-3940 (Print)
dc.identifier.doi10.1016/j.neulet.2006.01.015
dc.identifier.pmid16490315
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37626
dc.description.abstractThe potential neuroprotective effects of VELCADE were investigated in two different models of focal cerebral ischemia. For time-window assessment, male Wistar-Kyoto rats were treated with 0.2 mg/kg VELCADE at 1, 2, or 3 h after the induction of permanent middle cerebral artery occlusion (MCAO) using the suture occlusion method (experiment 1). To evaluate effects in a different model, male Sprague-Dawley rats received 0.2 mg/kg VELCADE after embolic MCAO (experiment 2). Infarct volume was calculated based on TTC-staining 24 h postischemia and whole blood proteasome activity was fluorometrically determined in both experiments at baseline, 1 and 24 h post-MCAO. In experiment 1, a dose of 0.2 mg/kg inhibited proteasome activity by 77% and infarct volume was reduced to 175.7+/-59.9 mm3 and 205.9+/-83.9 mm3 (1 and 2 h group, respectively; p<0.05) compared to 306.5+/-48.5 mm3 (control). Treatment at 3 h was not neuroprotective (293.0+/-40.1 mm3). After embolic MCAO, infarct volume was 167.5+/-90.7 mm3 (treatment group) and 398.9+/-141.3 mm3 (control; p=0.002). In conclusion, VELCADE treatment inhibited whole blood proteasome activity and achieved significant neuroprotection in two rat models of focal cerebral ischemia at various time points poststroke.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16490315&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.neulet.2006.01.015
dc.subjectAnimals
dc.subjectBoronic Acids
dc.subjectBrain Infarction
dc.subjectBrain Ischemia
dc.subjectDisease Models, Animal
dc.subjectInfarction, Middle Cerebral Artery
dc.subjectIntracranial Embolism
dc.subjectMale
dc.subjectNeuroprotective Agents
dc.subjectProteasome Endopeptidase Complex
dc.subjectPyrazines
dc.subjectRats
dc.subjectRats, Inbred WKY
dc.subjectRats, Sprague-Dawley
dc.subjectNeurology
dc.subjectNeuroscience and Neurobiology
dc.titleThe proteasome inhibitor VELCADE reduces infarction in rat models of focal cerebral ischemia
dc.typeJournal Article
dc.source.journaltitleNeuroscience letters
dc.source.volume398
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neuro_pp/169
dc.identifier.contextkey499351
html.description.abstract<p>The potential neuroprotective effects of VELCADE were investigated in two different models of focal cerebral ischemia. For time-window assessment, male Wistar-Kyoto rats were treated with 0.2 mg/kg VELCADE at 1, 2, or 3 h after the induction of permanent middle cerebral artery occlusion (MCAO) using the suture occlusion method (experiment 1). To evaluate effects in a different model, male Sprague-Dawley rats received 0.2 mg/kg VELCADE after embolic MCAO (experiment 2). Infarct volume was calculated based on TTC-staining 24 h postischemia and whole blood proteasome activity was fluorometrically determined in both experiments at baseline, 1 and 24 h post-MCAO. In experiment 1, a dose of 0.2 mg/kg inhibited proteasome activity by 77% and infarct volume was reduced to 175.7+/-59.9 mm3 and 205.9+/-83.9 mm3 (1 and 2 h group, respectively; p<0.05) compared to 306.5+/-48.5 mm3 (control). Treatment at 3 h was not neuroprotective (293.0+/-40.1 mm3). After embolic MCAO, infarct volume was 167.5+/-90.7 mm3 (treatment group) and 398.9+/-141.3 mm3 (control; p=0.002). In conclusion, VELCADE treatment inhibited whole blood proteasome activity and achieved significant neuroprotection in two rat models of focal cerebral ischemia at various time points poststroke.</p>
dc.identifier.submissionpathneuro_pp/169
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.contributor.departmentDepartment of Neurology
dc.source.pages300-5


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