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arachidonic acid/оток
Линкът е запазен в клипборда
Страница 1 от 668 резултата
Direct Involvement of Arachidonic Acid in the Development of Ear Edema via TRPV3.
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Arachidonic acid (AA) plays a pivotal role in the development of edema via its oxidized metabolites derived from cyclooxygenase (COX) and lipoxygenase (LOX), and is recently recognized as an activator of TRPV3. However, it is not clear whether AA plays some TRPV3-mediated pathological roles in the
Effect of anti-inflammatory compounds on edema formation and myeloperoxidase activity in the arachidonic acid-induced ear model in the mouse.
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The arachidonic acid (AA)-induced ear edema model in the mouse has been demonstrated as an effective in vivo experimental tool to screen compounds showing anti-inflammatory activity. Since neutrophil influx is a component of the inflammatory reaction, we have modified this assay by quantitating
Effects of indole-3-acetic acid on croton oil- and arachidonic acid-induced mouse ear edema.
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The indole-3-acetic acid (IAA) is a plant growth hormone (auxin) being considered as a tryptophan metabolite in animals. The main purpose of this work was to verify IAA's topical anti-inflammatory action using croton oil- or arachidonic acid-induced mouse ear edema, in comparison to known
[Inhibition of arachidonic acid-induced ear edema in the mouse with lipoxygenase-, cyclo-oxygenase- and dual inhibitors].
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The ear edema of the mouse induced by local application of arachidonic acid is suitable for in vivo differentiation of lipoxygenase (LOX) and cyclooxygenase (COX) inhibitors. LOX blockers inhibit initially and plateau-like during the first hour of the course of the edema, while COX-blockers do so
Role of arachidonic acid metabolism on ischemic brain edema and metabolism.
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Arachidonic acid is liberated from damaged cell membranes during ischemia and is the source of vasoactive prostanoids. In this study, specific drugs that influence AA metabolism were investigated for their effects on brain edema and energy metabolites during ischemia. The agents tested were:
Arachidonic acid metabolites mediate early burn edema.
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Standard burns were sequentially produced on the backs of Sprague-Dawley rats at 0, 1, 2, and 2 1/2 hr, followed by the IV injection of Evans blue dye. All animals were killed at 3 hr, and burns evaluated by wet/dry weight ratios, and Evans blue extravasation scored 1-4 by two observers. Five groups
Favorable combination effects of the leukotriene synthesis inhibitor BAY X 1005 and dexamethasone on edema formation in the arachidonic acid-induced mouse ear inflammation test.
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The effects of a combination of the leukotriene synthesis inhibitor (LSI) BAY X 1005 with the glucocorticosteroid dexamethasone were studied in the arachidonic acid (AA)-induced mouse ear inflammation test (AA-MEIT). We have determined the dose-dependent effects of dexamethasone to reduce edema
Inhibition of arachidonic acid-induced vasogenic brain edema by the non-glucocorticoid 21-aminosteroid U74006F.
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The effects of the novel non-glucocorticoid 21-aminosteroid U74006F on arachidonic acid (AA)-induced vasogenic brain edema were examined in rats. Vasogenic edema was assessed in terms of the extent of Evan's blue extravasation after subcortical micro-injection of AA indicative of blood-brain barrier
Alpha-human atrial natriuretic peptide (alpha-hANP) prevents pulmonary edema induced by arachidonic acid treatment in isolated perfused lung from guinea pig.
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Protective effect of alpha-human atrial natriuretic peptide (alpha-hANP) on pulmonary edema was investigated using an isolated perfused lung model. Infusion of alpha-hANP (1.7 to 22 ng/ml or 0.56 to 7.3 nM) prevented the edema induced in isolated lung from guinea pig by repeated treatment of 50
[Role of arachidonic acid metabolites on development of ischemic cerebral edema in rat middle cerebral artery occlusion].
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The products resulting from arachidonic acid metabolism of the both cyclo-oxygenase and lipoxygenase pathways possess strong physiological activities, such as vasoconstriction and the enhancement of vascular permeability. Therefore, it is likely that these metabolites are involved in cerebral
The pharmacology of arachidonic acid-induced rat paw edema.
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Arachidonic acid (AA) injected into hindpaws of Lewis rats produces a severe edematous response. Treatment with corticosteroids (dexamethasone, prednisolone), dual inhibitors of arachidonate metabolism (phenidone, SK & F 86002), anti-histamine/serotonin agents (chlorpheniramine, cyproheptadine) and
Cerebral edema induced by arachidonic acid: role of leukocytes and 5-lipoxygenase products.
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Arachidonic acid is released from cellular phospholipid membranes after brain injury associated with vasogenic edema. Intracerebral injection of arachidonic acid results in rapid breakdown of the blood-brain barrier, followed by an increase in brain water and sodium content. This effect is
[Simultaneous and sequential inhibition of the arachidonic acid cascade by inhibitors of phospholipase A2, cyclooxygenase and lipoxygenases in carrageenan edema and adjuvant arthritis in the rat].
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According to the aim of the simultaneous and sequential inhibition of key enzymes of the arachidonic acid cascade, combinations of inhibitors of the phospholipase A2 (PLA2), cyclooxygenase (COX) and of lipoxygenases (LOX) were administered to rats with carrageenin edema and adjuvant arthritis,
[Peroxidation of arachidonic acid and brain edema].
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Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the
Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung.
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We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The
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