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Effect of the proteasome inhibitor MLN519 on the expression of inflammatory molecules following middle cerebral artery occlusion and reperfusion in the rat

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Neurotoxicity Research : Volume 5, Issue 6, January 2003

Neurotoxicity Research : Volume 5, Issue 5, January 2003

Neurotoxicity Research : Volume 5, Issue 4, January 2003

Neurotoxicity Research : Volume 5, Issue 3, January 2003

Neurotoxicity Research : Volume 5, Issue 1-2, January 2003

Neurotoxicity Research : Volume 4

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Neurotoxicity Research : Volume 1

Effect of the proteasome inhibitor MLN519 on the expression of inflammatory molecules following middle cerebral artery occlusion and reperfusion in the rat

Content Provider	Springer Nature Link
Author	Berti, R. Williams, A. J. Velarde, L. C. Moffett, J. R. Elliott, P. J. Adams, J. Yao, C. Dave, J. R. Tortella, F. C.
Copyright Year	2003
Abstract	Anti-inflammatory treatment with the proteasome inhibitor MLN519 has been previously reported to be neuroprotective against ischemic brain injury in rats. These effects have been related to inhibition of the transcription factor NF-κB, which is activated through ubiquitin-proteasomal degradation. The aim of this study was to evaluate the effects of MLN519 to alter the expression of several inflammatory genes under the control of NF-κB. Male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAo) followed by vehicle or MLN519 (1.0 mg/kg, i.v.) treatment immediately after reperfusion of blood to the brain at 2h. Gene expression was evaluated 3–72 h post-MCAo. The most striking effects of intravenous treatment with MLN519 were associated with reductions in ICAM-1 expression at 3 h followed by reductions in E-selectin (12–72 h). Less dramatic reductions were observed in IL-1β (3–24h) and TNF-α (24 h) with no apparent effects on IL-6 and VCAM-1 mRNA levels. Immunohistochemical analysis revealed that the genes most dramatically affected by MLN519 had highest expression in endothelial cells and leukocytes (E-selectin, ICAM-1), indicating that these cell types may be the primary targets of intravenously delivered MLN519 treatment.
Starting Page	505
Ending Page	514
Page Count	10
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	5
Issue Number	7
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2003-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Middle cerebral artery occlusion inflammation ischemia stroke MLN519 NF-κB proteasome inhibition Neurosciences Pharmaceutical Sciences/Technology Neurology Neurochemistry Pharmacology/Toxicology Neurobiology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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