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cyclooxygenase/demam
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Specific roles of cyclooxygenase-1 and cyclooxygenase-2 in lipopolysaccharide-induced fever and Fos expression in rat brain.
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Fever is a coordinated autonomic, endocrine, and behavioral response mediated by the brain in reaction to inflammatory stimuli. An essential step in transmitting the immune signal to the brain is the formation of prostaglandin E2. Cyclooxygenase (COX) is the critical enzyme in the synthesis of
Lipopolysaccharide injected into the cerebral ventricle evokes fever through induction of cyclooxygenase-2 in brain endothelial cells.
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Activation of the arachidonic acid cascade is an essential step for the development of fever during brain inflammation. We investigated the brain sites where this activation takes place by use of a rat model of brain inflammation. Intracerebroventricular administration of lipopolysaccharide but not
Attenuated fever in pregnant rats is associated with blunted syntheses of brain cyclooxygenase-2 and PGE2.
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Attenuation of fever occurs in pregnant animals. This study examined a hypothesis that brain production of PGE(2), the final mediator of fever, is suppressed in pregnant animals. Near-term pregnant rats and age-matched nonpregnant female rats were injected with lipopolysaccharide (100 microg/kg)
Cyclooxygenase inhibition and hyperthermia for the potentiation of the cytotoxic response in ovarian cancer cells.
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OBJECTIVE
The progression of chemotherapy-resistant cancer confers poor prognosis and decreases overall survival in ovarian cancer patients. Adjuvants to traditional chemotherapy regimens have become attractive modalities for the clinical treatment of refractory or resistant ovarian cancer. We
The effects of selective and nonselective cyclooxygenase inhibitors on endothelin-1-induced fever in rats.
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It was previously shown that sustained fever can be induced in rats by central injection of endothelin-1 (ET-1). This peptide appears to participate in the mechanism(s) of LPS-induced fever, which is reduced by pretreatments with ET(B) receptor antagonists. In this study, we compared the effects of
Cyclooxygenase-2 inhibition by rofecoxib reverses naturally occurring fever in humans.
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Cyclooxygenase (COX) exists as constitutive (COX-1) and inducible (COX-2) isoforms. Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and diclofenac inhibit both COX-1 and COX-2. The role of COX-2 in the genesis of fever in monkeys and humans was examined with use of the specific COX-2
Interaction between inhibitors of inducible nitric oxide synthase and cyclooxygenase in Brewer's yeast induced pyrexia in mice: an isobolographic study.
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We studied the interaction of S-methylisothiourea (a selective inducible nitric oxide synthase inhibitor) with rofecoxib (selective cyclooxygenase-2 inhibitor) and mefenamic acid (non-selective cyclooxygenase inhibitor) in Brewer's yeast-induced pyrexia in mice by isobolographic analysis. Each drug
Cyclooxygenase inhibitors attenuate augmented glutamate release in organum vasculosum laminae terminalis and fever induced by staphylococcal enterotoxin A.
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Both the hyperthermia and augmented glutamate release in the organum vasculosum laminae terminalis (OVLT) after an intravenous dose (30 ng/kg) of staphylococcal enterotoxin A (SEA) were significantly reduced by pretreatment with intravenous administration of cyclooxygenase inhibitors such as aspirin
Endotoxin fever in granulocytopenic rats: evidence that brain cyclooxygenase-2 is more important than circulating prostaglandin E(2).
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PGE(2) is a recognized mediator of many fevers, and cyclooxygenase (COX) is the major therapeutic target for antipyretic therapy. The source, as well as the site of action of PGE(2), as an endogenous pyrogen, is widely accepted as being central, but PGE(2) in the circulation, possibly from
Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever.
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Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA)
Influence of systemic treatment with cyclooxygenase inhibitors on lipopolysaccharide-induced fever and circulating levels of cytokines and cortisol in guinea-pigs.
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Peripheral inflammatory stimuli result in the modification of a number of vital brain-controlled functions including the thermoregulatory set-point (induction of fever) and the activity of the hypothalamic-pituitary-adrenal (HPA) axis. We addressed the question of whether both of these components of
Cyclooxygenase-2 is induced in brain blood vessels during fever evoked by peripheral or central administration of tumor necrosis factor.
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Cyclooxygenase-2 (COX-2) is an inducible type of enzyme that is involved in prostaglandin biosynthesis. In the present study, we examined whether or not COX-2 is involved in fever that is induced by tumor necrosis factor-alpha (TNF-alpha) and, if so, where in the brain COX-2 is induced by this
Treatment of ragweed hay fever with flurbiprofen, a cyclooxygenase-inhibiting drug.
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Sixty-two volunteer hay fever patients participated in a 2-week trial which examined the protective effect of the cyclooxygenase-inhibiting drug flurbiprofen. The drug suppressed symptom severity significantly, though it was not as protective as the antihistamine also employed in the trial.
Intracisternal administration of transforming growth factor-beta evokes fever through the induction of cyclooxygenase-2 in brain endothelial cells.
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Transforming growth factor-beta (TGF-beta), a pleiotropic cytokine, regulates cell proliferation, differentiation, and apoptosis, and plays a key role in development and tissue homeostasis. TGF-beta functions as an anti-inflammatory cytokine because it suppresses microglia and B-lymphocyte
In vitro effects and in vivo efficacy of a novel cyclooxygenase-2 inhibitor in cats with lipopolysaccharide-induced pyrexia.
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OBJECTIVE
To determine cyclooxygenase (COX)-2 selectivity, pharmacokinetic properties, and in vivo efficacy of firocoxib (ML-1,785,713) in cats.
METHODS
5 healthy male and 14 healthy female domestic shorthair cats.
METHODS
Selectivity of firocoxib for inhibiting COX-2 was determined by comparing the
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