Essential Role of Inducible Nitric Oxide Synthase in Monophosphoryl Lipid A–Induced Late Cardioprotection
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منابع مشابه
Essential Role of Inducible Nitric Oxide Synthase in Monophosphoryl Lipid A
Mice Late Cardioprotection : Evidence From Pharmacological Inhibition and Gene Knockout Induced − Essential Role of Inducible Nitric Oxide Synthase in Monophosphoryl Lipid A Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1999 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: ...
متن کاملEssential role of inducible nitric oxide synthase in monophosphoryl lipid A-induced late cardioprotection: evidence from pharmacological inhibition and gene knockout mice.
BACKGROUND Monophosphoryl lipid A (MLA), a nontoxic analogue of endotoxin, is a pharmacological agent that is known to have anti-ischemic effects. Mechanisms involved with the cardioprotection are still unclear. A role for inducible nitric oxide synthase (iNOS) was recently proposed. We tested this hypothesis using S-methylisothiourea (SMT), one of the specific pharmacological inhibitors of iNO...
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Inducible nitric oxide synthase (iNOS) gene expresses a calcium calmudolin-independent enzyme which can catalyse NO production from L-arginine. The induction of iNOS activity has been demonstrated in a wide variety of cell types under stimulation with cytokines and lipopoly saccharide (LPS). Previous studies indicated that all nitric oxide synthases (NOS) activated in human umbilical vein endot...
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Objective(s):Some pathologic situations such as diabetes and metabolic syndrome are associated with alternation in nitric oxide level. Incidence of these condition increases with aging. On the other hand, insulin secretion is modulated by nitric oxide, and nitric oxide synthase (NOS) activity is also altered in diabetes. In this study, modification in the enzyme activity associated with aging a...
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ژورنال
عنوان ژورنال: Circulation
سال: 1999
ISSN: 0009-7322,1524-4539
DOI: 10.1161/01.cir.99.16.2157