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Mevastatin, an HMG-CoA Reductase Inhibitor, Reduces Stroke Damage and Upregulates Endothelial Nitric Oxide Synthase in Mice
Author(s) -
Sepideh AminHanjani,
Nancy E. Stagliano,
Masaru Yamada,
Paul L. Huang,
James K. Liao,
Michael A. Moskowitz
Publication year - 2001
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.32.4.980
Subject(s) - enos , medicine , cerebral blood flow , simvastatin , hmg coa reductase , middle cerebral artery , endocrinology , nitric oxide synthase , hydroxymethylglutaryl coa reductase , neuroprotection , stroke (engine) , statin , nitric oxide , ischemia , reductase , endothelial nos , cholesterol , biochemistry , biology , enzyme , engineering , mechanical engineering
The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) lower serum cholesterol and decrease the incidence of stroke and cardiovascular disease. There is growing evidence that statins exert some of their beneficial effects independent of cholesterol lowering. Indeed, we have previously demonstrated that chronic simvastatin administration upregulates endothelial nitric oxide synthase (eNOS), resulting in more functional protein, augmentation of cerebral blood flow, and neuroprotection in a murine model of cerebral ischemia. In this report we examined whether another member of the statin family shared these effects and whether eNOS upregulation is sustained with longer treatment.

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