lipoxygenase/edema

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Protective effect of the 5-lipoxygenase inhibitor AA-861 on cerebral edema after transient ischemia.

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This study examined the effect of AA-861, a specific 5-lipoxygenase inhibitor, on brain levels of leukotriene C4 (LTC4) and correlated any changes with changes in edema formation and cerebral blood flow (CBF) after transient ischemia in gerbils. Brain levels of LTC4 were observed to be increased at

Effect of antirheumatics and inhibitors of cyclooxygenase, lipoxygenases and thromboxane synthetase on cobra venom factor rat paw edema.

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The cobra venom factor (CVF) rat paw edema was inhibited by cyclooxygenase (indomethacin, piroxicam, aspirin), lipoxygenase (BW 755c) and thromboxane synthetase (imidazole) inhibitors as well as by dexamethasone and, at high doses, by paracetamol and phenacetin. No definite results were obtained

The mixed lipoxygenase/cyclooxygenase inhibitor SK&F 105809 reduces cerebral edema after closed head injury in rat.

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Closed head injury in rats induces edema formation, which is indicated by a decrease in cerebral specific gravity and an increase in water content. We previously described the activation of the eicosanoid metabolic cascade, namely, activation of PLA2 and accumulation of products of both

[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

Effects of lipoxygenase inhibitor on cerebral edema induced by freezing lesion in rats.

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This study was done to examine the effect of the lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA), on cerebral edema and to substantiate the hypothesis that the metabolites of arachidonic acid are involved in the pathogenesis of cerebral edema. The experiment was performed on rats with

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

Phorbol ester induction of 8-lipoxygenase in inbred SENCAR (SSIN) but not C57BL/6J mice correlated with hyperplasia, edema, and oxidant generation but not ornithine decarboxylase induction.

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Several responses suggested to be critical components of phorbol ester tumor promotion were compared in 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion-sensitive SSIN and TPA promotion-resistant C57BL/6J mice. SSIN mice treated topically with 2 micrograms of TPA showed extensive hyperplasia

[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,

A new 5-lipoxygenase selective inhibitor derived from Artocarpus communis strongly inhibits arachidonic acid-induced ear edema.

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Natural compounds isolated from the Indonesian plant, Artocarpus communis, inhibit 5-lipoxygenase of cultured mastocytoma cells. One of five compounds, AC-5-1, strongly inhibits 5-lipoxygenase with a half-inhibition dose of 5 +/- 0.12 X 10(-8) M. However, prostaglandin synthesizing activity is not

Modulation of mouse ear edema by cyclooxygenase and lipoxygenase inhibitors and other pharmacologic agents.

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Inhibitors of arachidonic acid (AA) metabolism and other pharmacologic agents were evaluated against ear edema produced in mice by tetradecanoylphorbol acetate (TPA) or AA. Drugs were administered orally and topically either 30 min prior to AA or 30 min after TPA, except for steroids which were

Effect of flavonol derivatives on the carrageenin-induced paw edema in the rat and inhibition of cyclooxygenase-1 and 5-lipoxygenase in vitro.

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Alkoxyflavonols were synthesized by the Algar-Flynn-Oyamada (AFO) cyclization of chalcones. Hydroxyflavonols were prepared by dealkylation of methoxyflavonols by refluxing in hydroiodic acid. The alkoxyflavonols 3-hydroxy-2-(2,3,4-trimethoxyphenyl)-4H-chromen-4-one (6),

Protecting against cerebrovascular injury: contributions of 12/15-lipoxygenase to edema formation after transient focal ischemia.

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OBJECTIVE The concept of the neurovascular unit suggests that effects on brain vasculature must be considered if neuroprotection is to be achieved in stroke. We previously reported that 12/15-lipoxygenase (12/15-LOX) is upregulated in the peri-infarct area after middle cerebral artery occlusion in

Intrapulmonary application of a 5-lipoxygenase inhibitor using surfactant as a carrier reduces lung edema in a piglet model of airway lavage.

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Leukotriene-generated effects on microvascular integrity and polymorphonuclear leukocytes (PMNL) play a key role in the inflammatory process of the alveolar-capillary unit in neonatal acute respiratory distress syndrome. We asked if intrapulmonary application of MK886, a 5-lipoxygenase inhibitor,

Effects of cyclooxygenase and lipoxygenase inhibitors on cerebral edema induced by freezing lesions in rats.

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The effects of indomethacin and/or nordihydroguaiaretic acid on cerebral edema were studied in rats with vasogenic edema induced by freezing lesions. The results demonstrated that the intracranial pressure, water content, and sodium and calcium but not potassium content were significantly decreased

Role of leukocytes and 5-lipoxygenase products in induction of cerebral edema.

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