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cyclooxygenase/stroke
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Melatonin reduces infarction volume in a photothrombotic stroke model in the wild-type but not cyclooxygenase-1-gene knockout mice.
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Cyclooxygenase (COX)-2 plays a harmful role in cerebral ischemic/reperfusion injury, but the role of COX-1 is uncertain. In the present study, cerebral infarct was induced by photothrombosis. Intraperitoneal injections of melatonin at 15 g/kg or its vehicle were made at 0.5 hr before stroke and 24
Mutations within the cyclooxygenase-1 gene in aspirin non-responders with recurrence of stroke.
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BACKGROUND
Aspirin is a common antiplatelet drug used in the prevention of ischemic stroke due to its inhibitory effect on platelet cyclooxygenase-1 (Cox-1). Patients can be categorized as either aspirin 'responders' or 'non-responders' depending on whether they are protected against a secondary
Cyclooxygenase-2 (COX-2) G-765C is a protective factor for coronary artery disease but not for ischemic stroke: a meta-analysis.
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OBJECTIVE
Previous case-control studies suggested the single nucleotide polymorphism of cyclooxygenase-2 (COX-2) gene (G-765C) is associated with coronary artery disease (CAD) and ischemic stroke. However, other studies did not confirm this relationship. The objective was to assess the relationship
Cyclooxygenase- and cytochrome P450-derived eicosanoids in stroke.
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Arachidonic acid (AA) is metabolized by cyclooxygenase (COX) and cytochrome P450 (CYP) enzymes into eicosanoids, which are involved in cardiovascular diseases and stroke. Evidence has demonstrated the important functions of these eicosanoids in regulating cerebral vascular tone, cerebral blood flow,
Cyclooxygenase-1 gene knockout does not alter middle cerebral artery occlusion in a mouse stroke model.
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Cyclooxygenase (COX) is crucial in inflammation; COX-1 is constitutional, and COX-2 is inducible. In this study, neurological function and infarct volume were evaluated at 24 h after permanent endovascular middle cerebral artery occlusion (MCAO) in both COX-1-gene knockout (homozygous or
Reduced expressions of inducible nitric oxide synthase and cyclooxygenase-2 in vascular smooth muscle cells of stroke-prone spontaneously hypertensive rats.
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Inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 are expressed in vascular smooth muscle cells stimulated with interleukin-1beta (IL-1beta), resulting in the production of nitric oxide (NO) and prostaglandins (PGs) such as PGI2. The iNOS and COX-2 proteins and their mRNA expressions
Upregulated expression of Toll-like receptor 4 in peripheral blood of ischaemic stroke patients correlates with cyclooxygenase 2 expression.
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OBJECTIVE
An inflammatory process following stroke in human brains and systemic inflammatory responses after stroke in humans have been reported by numerous investigators. The aim of the study was to investigate if genes involved in the cyclooxygenase 2 (COX-2) pathway are upregulated at peripheral
Microglia and cyclooxygenase-2: possible therapeutic targets of progesterone for stroke.
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Previous studies have demonstrated that progesterone (PROG) may be a pleiotropic neuroprotective agent. Although there have been reports about the neurotoxicity of activated microglia and cyclooxygenase-2 (COX-2) in animal models of ischemic stroke, the influence of PROG on the activation of
Increased risk of incident stroke associated with the cyclooxygenase 2 (COX-2) G-765C polymorphism in African-Americans: the Atherosclerosis Risk in Communities Study.
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BACKGROUND
A hallmark feature of atherosclerosis is inflammation mediated by prostaglandins (PGs) catalyzed by the enzyme cyclooxygenase (COX). The present study explored whether the COX-2 G-765C polymorphism contributes to increased incidence of coronary heart disease (CHD) or stroke in the large
Influence of cyclooxygenase-1 genotype on ex vivo aspirin response in patients at risk for stroke.
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BACKGROUND
We sought to determine whether cyclooxygenase-1 (PTGS1) genotype is associated with the ability of aspirin to inhibit platelet aggregation in patients at risk for stroke.
METHODS
Blood and urine samples were collected from 60 subjects, including 28 African Americans, who were taking
Cyclooxygenase-2 selective nonsteroidal anti-inflammatory drugs and the risk of ischemic stroke: a nested case-control study.
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OBJECTIVE
Several randomized trials and a large number of epidemiological studies have provided evidence of an increased risk of acute myocardial infarction associated with the use of cyclooxygenase (COX)-2 selective nonsteroidal anti-inflammatory drugs (NSAIDs). Few data are available concerning
Chronic inhibition of cyclooxygenase-2 induces dendritic hypertrophy and limited functional improvement following motor cortex stroke.
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The cyclooxygenase-2 (COX-2) enzyme is part of the inflammatory pathway and is induced within the brain by a variety of pathological events, including ischemia. Pharmacological agents that inhibit COX-2 have been found to be neuroprotective in a number of injury models, and long-term administration
Cyclooxygenase-2 selectivity of non-steroidal anti-inflammatory drugs and the risk of myocardial infarction and cerebrovascular accident.
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OBJECTIVE
To assess degree of cyclooxygenase-2 (COX-2) selectivity of a non-steroidal anti-inflammatory drug (NSAID) and risk of myocardial infarction (MI) or cerebrovascular accident (CVA).
METHODS
Prescription fill data were linked to medical records of a merged VA-Medicare dataset. NSAIDs were
Flavocoxid, dual inhibitor of cyclooxygenase-2 and 5-lipoxygenase, exhibits neuroprotection in rat model of ischaemic stroke.
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The efficacy of flavocoxid, a prescription medical food used in osteoarthritis in the USA, containing natural flavonoids, baicalin and catechin in experimentally induced cerebral ischaemia in rats was evaluated. Rationale behind the study was that the transient acute ischaemic attack triggers
A polymorphism in the cyclooxygenase 2 gene as an inherited protective factor against myocardial infarction and stroke.
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BACKGROUND
Myocardial infarction (MI) and ischemic stroke are thought to be caused by matrix digestion by metalloproteinases (MMPs) leading to rupture of atherosclerotic plaques. Production of macrophage MMP-2 and MMP-9 is induced by cyclooxygenase 2 (COX-2) and prostaglandin E(2) synthesis.
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